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At the heart of programming: the role of micro-RNAs

Part of: French DOHaD DOHaD on International Women's Day 2020

Published online by Cambridge University Press:  18 June 2018

B. Siddeek ,
C. Mauduit ,
C. Yzydorczyk ,
M. Benahmed  and
U. Simeoni
B. Siddeek*
Affiliation:
Woman-Mother-Child-Department, Division of Pediatrics, DOHaD Laboratory, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
C. Mauduit
Affiliation:
INSERM U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), Team 5, Nice, France
C. Yzydorczyk
Affiliation:
Woman-Mother-Child-Department, Division of Pediatrics, DOHaD Laboratory, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
M. Benahmed
Affiliation:
INSERM U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), Team 5, Nice, France
U. Simeoni
Affiliation:
Woman-Mother-Child-Department, Division of Pediatrics, DOHaD Laboratory, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
*
Address for correspondence: Benazir Siddeek, Woman-Mother-Child-Department, Division of Pediatrics, DOHaD Laboratory, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Rue du Bugnon 27, 1011, Lausanne, Switzerland. E-mail: [email protected]
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Abstract

Epidemiological and experimental observations tend to prove that environment, lifestyle or nutritional challenges influence heart functions together with genetic factors. Furthermore, when occurring during sensitive windows of heart development, these environmental challenges can induce an ‘altered programming’ of heart development and shape the future heart disease risk. In the etiology of heart diseases driven by environmental challenges, epigenetics has been highlighted as an underlying mechanism, constituting a bridge between environment and heart health. In particular, micro-RNAs which are involved in each step of heart development and functions seem to play a crucial role in the unfavorable programming of heart diseases. This review describes the latest advances in micro-RNA research in heart diseases driven by early exposure to challenges and discusses the use of micro-RNAs as potential targets in the reversal of the pathophysiology.

Keywords

cardio-metabolic dysfunctionsmicro-RNAsprogrammingreversal
Type
Review
Information
Journal of Developmental Origins of Health and Disease , Volume 9 , Issue 6 , December 2018 , pp. 615 - 631
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2018 

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References

1. Marín-García, J. Post-Genomic Cardiology. 2014. Elsevier Science: Cambridge, MA.Google Scholar
2. Thornburg, K, Jonker, S, O’Tierney, P, et al. Regulation of the cardiomyocyte population in the developing heart. Prog Biophys Mol Biol. 2011; 106, 289–299.Google Scholar
3. Van Berlo, JH, Molkentin, JD. An emerging consensus on cardiac regeneration. Nat Med. 2014; 20, 1386–1393.Google Scholar
4. Bubb, KJ, Cock, ML, Black, MJ, et al. Intrauterine growth restriction delays cardiomyocyte maturation and alters coronary artery function in the fetal sheep. J Physiol. 2007; 578, 871–881.Google Scholar
5. Nakano, H, Minami, I, Braas, D, et al. Glucose inhibits cardiac muscle maturation through nucleotide biosynthesis. eLife. 2017; 6, e29330.Google Scholar
6. Buyon, JP, Swersky, SH, Fox, HE, Bierman, FZ, Winchester, RJ. Intrauterine therapy for presumptive fetal myocarditis with acquired heart block due to systemic lupus erythematosus. Experience in a mother with a predominance of SS-B (La) antibodies. Arthritis Rheum. 1987; 30, 44–49.Google Scholar
7. Cole, CR, Yutzey, KE, Brar, AK, et al. Congenital heart disease linked to maternal autoimmunity against cardiac myosin. J Immunol. 2014; 192, 4074–4082.Google Scholar
8. Mills, JL, Troendle, J, Conley, MR, Carter, T, Druschel, CM. Maternal obesity and congenital heart defects: a population-based study. Am J Clin Nutr. 2010; 91, 1543–1549.Google Scholar
9. Savarese, G, Lund, LH. Global public health burden of heart failure. Card Fail Rev. 2017; 3, 7–11.Google Scholar
10. Ghouse, J, Skov, MW, Bigseth, RS, Ahlberg, G, Kanters, JK, Olesen, MS. Distinguishing pathogenic mutations from background genetic noise in cardiology: the use of large genome databases for genetic interpretation. Clin Genet. 2018; 93, 459–466.Google Scholar
11. Nolte, IM, Munoz, ML, Tragante, V, et al. Genetic loci associated with heart rate variability and their effects on cardiac disease risk. Nat Commun. 2017; 8, 15805.Google Scholar
12. Lin, Q, Schwarz, J, Bucana, C, Olson, EN. Control of mouse cardiac morphogenesis and myogenesis by transcription factor MEF2C. Science. 1997; 276, 1404–1407.Google Scholar
13. Tzimas, C, Johnson, DM, Santiago, DJ, et al. Impaired calcium homeostasis is associated with sudden cardiac death and arrhythmias in a genetic equivalent mouse model of the human HRC-Ser96Ala variant. Cardiovasc Res. 2017; 113, 1403–1417.Google Scholar
14. Ruggiero, A, Chen, SN, Lombardi, R, Rodriguez, G, Marian, AJ. Pathogenesis of hypertrophic cardiomyopathy caused by myozenin 2 mutations is independent of calcineurin activity. Cardiovasc Res. 2013; 97, 44–54.Google Scholar
15. Slingo, M, Cole, M, Carr, C, et al. The von Hippel-Lindau Chuvash mutation in mice alters cardiac substrate and high-energy phosphate metabolism. Am J Physiol Heart Circ Physiol. 2016; 311, H759–H767.Google Scholar
16. Crotti, L, Johnson, CN, Graf, E, et al. Calmodulin mutations associated with recurrent cardiac arrest in infants. Circulation. 2013; 127, 1009–1017.Google Scholar
17. Dorn, G, Triposkiadis, F, Karayannis, G, Giamouzis, G, Skoularigis, J, Louridas, G, Butler, J. Adrenergic signaling polymorphisms and their impact on cardiovascular disease. Physiol Rev. 2010; 90, 1013–1062.Google Scholar
18. Liggett, SB, Cresci, S, Kelly, RJ, et al. A GRK5 polymorphism that inhibits beta-adrenergic receptor signaling is protective in heart failure. Nat Med. 2008; 14, 510–517.Google Scholar
19. Danser, AH, Schalekamp, MA, Bax, WA, et al. Angiotensin-converting enzyme in the human heart. Effect of the deletion/insertion polymorphism. Circulation. 1995; 92, 1387–1388.Google Scholar
20. Bai, Y, Wang, L, Hu, S, Wei, Y. Association of angiotensin-converting enzyme I/D polymorphism with heart failure: a meta-analysis. Mol Cell Biochem. 2012; 361, 297–304.Google Scholar
21. Humblet, O, Birnbaum, L, Rimm, E, Mittleman, MA, Hauser, R. Dioxins and cardiovascular disease mortality. Environ Health Perspect. 2008; 116, 1443–1448.Google Scholar
22. Yan, S, Song, W, Chen, Y, Hong, K, Rubinstein, J, Wang, HS. Low-dose bisphenol A and estrogen increase ventricular arrhythmias following ischemia-reperfusion in female rat hearts. Food Chem Toxicol. 2013; 56, 75–80.Google Scholar
23. Dzhambov, AM, Dimitrova, DD. Heart disease attributed to occupational noise, vibration and other co-exposure: self-reported population-based survey among Bulgarian workers. Med Pr. 2016; 67, 435–445.Google Scholar
24. Pan, WH, Li, LA, Tsai, MJ. Temperature extremes and mortality from coronary heart disease and cerebral infarction in elderly Chinese. Lancet. 1995; 345, 353–355.Google Scholar
25. Pharr, JR, Coughenour, CA, Bungum, TJ. An assessment of the relationship of physical activity, obesity, and chronic diseases/conditions between active/obese and sedentary/normal weight American women in a national sample. Public Health. 2018; 156, 117–123.Google Scholar
26. Arsenault, BJ, Rana, JS, Lemieux, I, et al. Physical inactivity, abdominal obesity and risk of coronary heart disease in apparently healthy men and women. Int J Obes (Lond). 2010; 34, 340–347.Google Scholar
27. Iribarren, C, Tekawa, IS, Sidney, S, Friedman, GD. Effect of cigar smoking on the risk of cardiovascular disease, chronic obstructive pulmonary disease, and cancer in men. N Engl J Med. 1999; 340, 1773–1780.Google Scholar
28. Catena, C, Colussi, G, Verheyen, ND, et al. Moderate alcohol consumption is associated with left ventricular diastolic dysfunction in nonalcoholic hypertensive patients. Hypertension. 2016; 68, 1208–1216.Google Scholar
29. Park, SK, Moon, K, Ryoo, JH, et al. The association between alcohol consumption and left ventricular diastolic function and geometry change in general Korean population. Eur Heart J Cardiovasc Imaging. 2018; 19, 271–278.Google Scholar
30. Brunner, S, Herbel, R, Drobesch, C, et al. Alcohol consumption, sinus tachycardia, and cardiac arrhythmias at the Munich Octoberfest: results from the Munich Beer Related Electrocardiogram Workup Study (MunichBREW). Eur Heart J. 2017; 38, 2100–2106.Google Scholar
31. Wang, Z, Li, L, Zhao, H, Peng, S, Zuo, Z. Chronic high fat diet induces cardiac hypertrophy and fibrosis in mice. Metabolism. 2015; 64, 917–925.Google Scholar
32. Hall, ME, Harmancey, R, Stec, DE. Lean heart: role of leptin in cardiac hypertrophy and metabolism. World J Cardiol. 2015; 7, 511–524.Google Scholar
33. Bobbert, P, Jenke, A, Bobbert, T, et al. High leptin and resistin expression in chronic heart failure: adverse outcome in patients with dilated and inflammatory cardiomyopathy. Eur J Heart Fail. 2012; 14, 1265–1275.Google Scholar
34. Christoffersen, C, Bollano, E, Lindegaard, ML, et al. Cardiac lipid accumulation associated with diastolic dysfunction in obese mice. Endocrinology. 2003; 144, 3483–3490.Google Scholar
35. Kankaanpaa, M, Lehto, HR, Parkka, JP, et al. Myocardial triglyceride content and epicardial fat mass in human obesity: relationship to left ventricular function and serum free fatty acid levels. J Clin Endocrinol Metab. 2006; 91, 4689–4695.Google Scholar
36. Trichopoulos, D, Katsouyanni, K, Zavitsanos, X, Tzonou, A, Dalla-Vorgia, P. Psychological stress and fatal heart attack: the Athens (1981) earthquake natural experiment. Lancet. 1983; 1, 441–444.Google Scholar
37. Kark, JD, Goldman, S, Epstein, L. Iraqi missile attacks on Israel. The association of mortality with a life-threatening stressor. JAMA. 1995; 273, 1208–1210.Google Scholar
38. Ruidavets, JB, Paterniti, S, Bongard, V, Giroux, M, Cassadou, S, Ferrieres, J. Triggering of acute coronary syndromes after a chemical plant explosion. Heart. 2006; 92, 257–258.Google Scholar
39. Chandola, T, Britton, A, Brunner, E, et al. Work stress and coronary heart disease: what are the mechanisms? Eur Heart J. 2008; 29, 640–648.Google Scholar
40. Auger, N, Fraser, WD, Sauve, R, Bilodeau-Bertrand, M, Kosatsky, T. Risk of congenital heart defects after ambient heat exposure early in pregnancy. Environ Health Perspect. 2017; 125, 8–14.Google Scholar
41. Brain, KL, Allison, BJ, Niu, Y, et al. Induction of controlled hypoxic pregnancy in large mammalian species. Physiol Rep. 2015; 3, e12614.Google Scholar
42. Giussani, DA, Camm, EJ, Niu, Y, et al. Developmental programming of cardiovascular dysfunction by prenatal hypoxia and oxidative stress. PLoS One. 2012; 7, e31017.Google Scholar
43. Forsen, T, Eriksson, JG, Tuomilehto, J, Teramo, K, Osmond, C, Barker, DJ. Mother’s weight in pregnancy and coronary heart disease in a cohort of Finnish men: follow up study. BMJ. 1997; 315, 837–840.Google Scholar
44. Roseboom, T, De Rooij, S, Painter, R. The Dutch famine and its long-term consequences for adult health. Early Hum Dev. 2006; 82, 485–491.Google Scholar
45. Tintu, A, Rouwet, E, Verlohren, S, et al. Hypoxia induces dilated cardiomyopathy in the chick embryo: mechanism, intervention, and long-term consequences. PLoS One. 2009; 4, e5155.Google Scholar
46. Botting, KJ, McMillen, IC, Forbes, H, Nyengaard, JR, Morrison, JL. Chronic hypoxemia in late gestation decreases cardiomyocyte number but does not change expression of hypoxia-responsive genes. J Am Heart Assoc. 2014; 3, e000531.Google Scholar
47. Rueda-Clausen, CF, Morton, JS, Lopaschuk, GD, Davidge, ST. Long-term effects of intrauterine growth restriction on cardiac metabolism and susceptibility to ischaemia/reperfusion. Cardiovasc Res. 2011; 90, 285–294.Google Scholar
48. Kuo, AH, Li, C, Li, J, Huber, HF, Nathanielsz, PW, Clarke, GD. Cardiac remodelling in a baboon model of intrauterine growth restriction mimics accelerated ageing. J Physiol. 2017; 595, 1093–1110.Google Scholar
49. Li, G, Xiao, Y, Estrella, JL, Ducsay, CA, Gilbert, RD, Zhang, L. Effect of fetal hypoxia on heart susceptibility to ischemia and reperfusion injury in the adult rat. J Soc Gynecol Investig. 2003; 10, 265–274.Google Scholar
50. Wang, KC, Zhang, L, McMillen, IC, et al. Fetal growth restriction and the programming of heart growth and cardiac insulin-like growth factor 2 expression in the lamb. J Physiol. 2011; 589, 4709–4722.Google Scholar
51. Wang, KC, Tosh, DN, Zhang, S, et al. IGF-2R-Galphaq signaling and cardiac hypertrophy in the low-birth-weight lamb. Am J Physiol Regul Integr Comp Physiol. 2015; 308, R627–R635.Google Scholar
52. Lin, X, Yang, P, Reece, EA, Yang, P. Pregestational type 2 diabetes mellitus induces cardiac hypertrophy in the murine embryo through cardiac remodeling and fibrosis. Am J Obstet Gynecol. 2017; 217, 216.e1–216.e13.Google Scholar
53. Martins, MR, Vieira, AK, de Souza, EP, Moura, AS. Early overnutrition impairs insulin signaling in the heart of adult Swiss mice. J Endocrinol. 2008; 198, 591–598.Google Scholar
54. Borradaile, NM, Schaffer, JE. Lipotoxicity in the heart. Curr Hypertens Rep. 2005; 7, 412–417.Google Scholar
55. Fiorino, P, Americo, AL, Muller, CR, et al. Exposure to high-fat diet since post-weaning induces cardiometabolic damage in adult rats. Life Sci. 2016; 160, 12–17.Google Scholar
56. King, V, Norman, JE, Seckl, JR, Drake, AJ. Post-weaning diet determines metabolic risk in mice exposed to overnutrition in early life. Reprod Biol Endocrinol. 2014; 12, 73.Google Scholar
57. Fang, X, Poulsen, RR, Rivkees, SA, Wendler, CC. In utero caffeine exposure induces transgenerational effects on the adult heart. Sci Rep. 2016; 6, 34106.Google Scholar
58. Nguyen, VB, Probyn, ME, Campbell, F, et al. Low-dose maternal alcohol consumption: effects in the hearts of offspring in early life and adulthood. Physiol Rep. 2014; 2, e12087.Google Scholar
59. Reitan, T, Callinan, S. Changes in smoking rates among pregnant women and the general female population in Australia, Finland, Norway, and Sweden. Nicotine Tob Res. 2017; 19, 282–289.Google Scholar
60. Butler, NR, Goldstein, H, Ross, EM. Cigarette smoking in pregnancy: its influence on birth weight and perinatal mortality. Br Med J. 1972; 2, 127–130.Google Scholar
61. Coste, J, Job-Spira, N, Fernandez, H. Increased risk of ectopic pregnancy with maternal cigarette smoking. Am J Public Health. 1991; 81, 199–201.Google Scholar
62. Ton, AT, Biet, M, Delabre, JF, Morin, N, Dumaine, R. In-utero exposure to nicotine alters the development of the rabbit cardiac conduction system and provides a potential mechanism for sudden infant death syndrome. Arch Toxicol. 2017; 91, 3947–3960.Google Scholar
63. Makino, I, Matsuda, Y, Yoneyama, M, et al. Effect of maternal stress on fetal heart rate assessed by vibroacoustic stimulation. J Int Med Res. 2009; 37, 1780–1788.Google Scholar
64. Sanders, BJ, Anticevic, A. Maternal separation enhances neuronal activation and cardiovascular responses to acute stress in borderline hypertensive rats. Behav Brain Res. 2007; 183, 25–30.Google Scholar
65. Alastalo, H, Raikkonen, K, Pesonen, AK, et al. Cardiovascular morbidity and mortality in Finnish men and women separated temporarily from their parents in childhood – a life course study. Psychosom Med. 2012; 74, 583–587.Google Scholar
66. Aragon, AC, Kopf, PG, Campen, MJ, Huwe, JK, Walker, MK. In utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure: effects on fetal and adult cardiac gene expression and adult cardiac and renal morphology. Toxicol Sci. 2008; 101, 321–330.Google Scholar
67. Thackaberry, EA, Nunez, BA, Ivnitski-Steele, ID, Friggins, M, Walker, MK. Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on murine heart development: alteration in fetal and postnatal cardiac growth, and postnatal cardiac chronotropy. Toxicol Sci. 2005; 88, 242–249.Google Scholar
68. Chapalamadugu, KC, Vandevoort, CA, Settles, ML, Robison, BD, Murdoch, GK. Maternal bisphenol a exposure impacts the fetal heart transcriptome. PLoS One. 2014; 9, e89096.Google Scholar
69. MohanKumar, SM, Rajendran, TD, Vyas, AK, et al. Effects of prenatal bisphenol-A exposure and postnatal overfeeding on cardiovascular function in female sheep. J Dev Orig Health Dis. 2017; 8, 65–74.Google Scholar
70. Valenzuela-Alcaraz, B, Crispi, F, Bijnens, B, et al. Assisted reproductive technologies are associated with cardiovascular remodeling in utero that persists postnatally. Circulation. 2013; 128, 1442–1450.Google Scholar
71. Scherrer, U, Rexhaj, E, Allemann, Y, Sartori, C, Rimoldi, SF. Cardiovascular dysfunction in children conceived by assisted reproductive technologies. Eur Heart J. 2015; 36, 1583–1589.Google Scholar
72. Materna-Kiryluk, A, Wisniewska, K, Badura-Stronka, M, et al. Parental age as a risk factor for isolated congenital malformations in a Polish population. Paediatr Perinat Epidemiol. 2009; 23, 29–40.Google Scholar
73. Su, XJ, Yuan, W, Huang, GY, Olsen, J, Li, J. Paternal age and offspring congenital heart defects: a national cohort study. PLoS One. 2015; 10, e0121030.Google Scholar
74. Keverne, EB. Genomic imprinting, action, and interaction of maternal and fetal genomes. Proc Natl Acad Sci U S A. 2014; 112, 6834–6840.Google Scholar
75. Hughes, V. Epigenetics: the sins of the father. Nature. 2014; 507, 22–24.Google Scholar
76. Kaati, G, Bygren, LO, Edvinsson, S. Cardiovascular and diabetes mortality determined by nutrition during parents’ and grandparents’ slow growth period. Eur J Hum Genet. 2002; 10, 682–688.Google Scholar
77. Bartel, DP. MicroRNAs: genomics, biogenesis, mechanism, and function. Cell. 2004; 116, 281–297.Google Scholar
78. Martinez, SR, Gay, MS, Zhang, L. Epigenetic mechanisms in heart development and disease. Drug Discov Today. 2015; 20, 799–811.Google Scholar
79. Sandovici, I, Smith, NH, Nitert, MD, et al. Maternal diet and aging alter the epigenetic control of a promoter-enhancer interaction at the Hnf4a gene in rat pancreatic islets. Proc Natl Acad Sci U S A. 2011; 108, 5449–5454.Google Scholar
80. Yan, S, Jiao, K. Functions of miRNAs during mammalian heart development. Int J Mol Sci. 2016; 17, 789.Google Scholar
81. Latronico, MV, Condorelli, G. MicroRNAs and cardiac pathology. Nat Rev Cardiol. 2009; 6, 419–429.Google Scholar
82. Frost, RJ, Olson, EN. Control of glucose homeostasis and insulin sensitivity by the Let-7 family of microRNAs. Proc Natl Acad Sci U S A. 2011; 108, 21075–21080.Google Scholar
83. Trajkovski, M, Hausser, J, Soutschek, J, et al. MicroRNAs 103 and 107 regulate insulin sensitivity. Nature. 2011; 474, 649–653.Google Scholar
84. Lee, CT, Risom, T, Strauss, WM. Evolutionary conservation of microRNA regulatory circuits: an examination of microRNA gene complexity and conserved microRNA-target interactions through metazoan phylogeny. DNA Cell Biol. 2007; 26, 209–218.Google Scholar
85. Friedman, RC, Farh, KK, Burge, CB, Bartel, DP. Most mammalian mRNAs are conserved targets of microRNAs. Genome Res. 2009; 19, 92–105.Google Scholar
86. Lee, Y, Kim, M, Han, J, et al. MicroRNA genes are transcribed by RNA polymerase II. EMBO J. 2004; 23, 4051–4060.Google Scholar
87. Borchert, GM, Lanier, W, Davidson, BL. RNA polymerase III transcribes human microRNAs. Nat Struct Mol Biol. 2006; 13, 1097–1101.Google Scholar
88. Han, J, Lee, Y, Yeom, KH, Kim, YK, Jin, H, Kim, VN. The Drosha-DGCR8 complex in primary microRNA processing. Genes Dev. 2004; 18, 3016–3027.Google Scholar
89. Yi, R, Qin, Y, Macara, IG, Cullen, BR. Exportin-5 mediates the nuclear export of pre-microRNAs and short hairpin RNAs. Genes Dev. 2003; 17, 3011–3016.Google Scholar
90. Wilson, RC, Tambe, A, Kidwell, MA, Noland, CL, Schneider, CP, Doudna, JA. Dicer-TRBP complex formation ensures accurate mammalian microRNA biogenesis. Mol Cell. 2015; 57, 397–407.Google Scholar
91. Maniataki, E, Mourelatos, Z. A human, ATP-independent, RISC assembly machine fueled by pre-miRNA. Genes Dev. 2005; 19, 2979–2990.Google Scholar
92. Place, RF, Li, LC, Pookot, D, Noonan, EJ, Dahiya, R. MicroRNA-373 induces expression of genes with complementary promoter sequences. Proc Natl Acad Sci U S A. 2008; 105, 1608–1613.Google Scholar
93. Bruno, IG, Karam, R, Huang, L, et al. Identification of a microRNA that activates gene expression by repressing nonsense-mediated RNA decay. Mol Cell. 2011; 42, 500–510.Google Scholar
94. Atambayeva, S, Niyazova, R, Ivashchenko, A, et al. The binding sites of miR-619-5p in the mRNAs of human and orthologous genes. BMC Genomics. 2017; 18, 428.Google Scholar
95. Davis, CD, Ross, SA. Evidence for dietary regulation of microRNA expression in cancer cells. Nutr Rev. 2008; 66, 477–482.Google Scholar
96. Fiedler, SD, Carletti, MZ, Hong, X, Christenson, LK. Hormonal regulation of microRNA expression in periovulatory mouse mural granulosa cells. Biol Reprod. 2008; 79, 1030–1037.Google Scholar
97. Kulshreshtha, R, Ferracin, M, Negrini, M, Calin, GA, Davuluri, RV, Ivan, M. Regulation of microRNA expression: the hypoxic component. Cell Cycle. 2007; 6, 1426–1431.Google Scholar
98. Siddeek, B, Inoubli, L, Lakhdari, N, et al. MicroRNAs as potential biomarkers in diseases and toxicology. Mutat Res Genet Toxicol Environ Mutagen. 2014; 764-765, 46–57.Google Scholar
99. da Costa Martins, PA, Bourajjaj, M, Gladka, M, et al. Conditional dicer gene deletion in the postnatal myocardium provokes spontaneous cardiac remodeling. Circulation. 2008; 118, 1567–1576.Google Scholar
100. Chen, JF, Murchison, EP, Tang, R, et al. Targeted deletion of Dicer in the heart leads to dilated cardiomyopathy and heart failure. Proc Natl Acad Sci U S A. 2008; 105, 2111–2116.Google Scholar
101. Saxena, A, Tabin, CJ. miRNA-processing enzyme Dicer is necessary for cardiac outflow tract alignment and chamber septation. Proc Natl Acad Sci U S A. 2010; 107, 87–91.Google Scholar
102. Bernstein, E, Kim, SY, Carmell, MA, et al. Dicer is essential for mouse development. Nat Genet. 2003; 35, 215–217.Google Scholar
103. Wang, DZ. MicroRNAs in cardiac development and remodeling. Pediatr Cardiol. 2010; 31, 357–362.Google Scholar
104. Rottiers, V, Naar, AM. MicroRNAs in metabolism and metabolic disorders. Nat Rev Mol Cell Biol. 2012; 13, 239–250.Google Scholar
105. Yang, L, Li, Y, Wang, X, et al. Overexpression of miR-223 tips the balance of pro- and anti-hypertrophic signaling cascades toward physiologic cardiac hypertrophy. J Biol Chem. 2016; 291, 15700–15713. https://doi.org/10.1074/jbc.M116.715805.Google Scholar
106. Wang, H, Cai, J. The role of microRNAs in heart failure. Biochim Biophys Acta. 2017; 1863, 2019–2030.Google Scholar
107. Zhao, Y, Samal, E, Srivastava, D. Serum response factor regulates a muscle-specific microRNA that targets Hand2 during cardiogenesis. Nature. 2005; 436, 214–220.Google Scholar
108. Qian, L, Wythe, JD, Liu, J, et al. Tinman/Nkx2-5 acts via miR-1 and upstream of Cdc42 to regulate heart function across species. J Cell Biol. 2011; 193, 1181–1196.Google Scholar
109. Chen, J, Yin, H, Jiang, Y, et al. Induction of microRNA-1 by myocardin in smooth muscle cells inhibits cell proliferation. Arterioscler Thromb Vasc Biol. 2011; 31, 368–375.Google Scholar
110. Kwon, C, Han, Z, Olson, EN, Srivastava, D. MicroRNA1 influences cardiac differentiation in Drosophila and regulates Notch signaling. Proc Natl Acad Sci U S A. 2005; 102, 18986–18991.Google Scholar
111. Ali, R, Huang, Y, Maher, SE, et al. miR-1 mediated suppression of Sorcin regulates myocardial contractility through modulation of Ca2+ signaling. J Mol Cell Cardiol. 2012; 52, 1027–1037.Google Scholar
112. Zhao, Y, Ransom, JF, Li, A, et al. Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2. Cell. 2007; 129, 303–317.Google Scholar
113. Besser, J, Malan, D, Wystub, K, et al. MiRNA-1/133a clusters regulate adrenergic control of cardiac repolarization. PLoS One. 2014; 9, e113449.Google Scholar
114. Curcio, A, Torella, D, Iaconetti, C, et al. MicroRNA-1 downregulation increases connexin 43 displacement and induces ventricular tachyarrhythmias in rodent hypertrophic hearts. PLoS One. 2013; 8, e70158.Google Scholar
115. Rau, F, Freyermuth, F, Fugier, C, et al. Misregulation of miR-1 processing is associated with heart defects in myotonic dystrophy. Nat Struct Mol Biol. 2011; 18, 840–845.Google Scholar
116. Costantino, S, Paneni, F, Luscher, TF, Cosentino, F. MicroRNA profiling unveils hyperglycaemic memory in the diabetic heart. Eur Heart J. 2016; 37, 572–576.Google Scholar
117. De Gonzalo-Calvo, D, Van der Meer, RW, Rijzewijk, LJ, et al. Serum microRNA-1 and microRNA-133a levels reflect myocardial steatosis in uncomplicated type 2 diabetes. Sci Rep. 2017; 7, 47.Google Scholar
118. Rawal, S, Ram, TP, Coffey, S, et al. Differential expression pattern of cardiovascular microRNAs in the human type-2 diabetic heart with normal ejection fraction. Int J Cardiol. 2016; 202, 40–43.Google Scholar
119. Zampetaki, A, Kiechl, S, Drozdov, I, et al. Plasma microRNA profiling reveals loss of endothelial miR-126 and other microRNAs in type 2 diabetes. Circ Res. 2010; 107, 810–817.Google Scholar
120. Flowers, E, Aouizerat, BE, Abbasi, F, et al. Circulating microRNA-320a and microRNA-486 predict thiazolidinedione response: moving towards precision health for diabetes prevention. Metabolism. 2015; 64, 1051–1059.Google Scholar
121. Liu, X, You, L, Zhou, R, Zhang, J. Significant association between functional microRNA polymorphisms and coronary heart disease susceptibility: a comprehensive meta-analysis involving 16484 subjects. Oncotarget. 2017; 8, 5692–5702.Google Scholar
122. Lock, MC, Botting, KJ, Tellam, RL, Brooks, D, Morrison, JL. Adverse intrauterine environment and cardiac miRNA expression. Int J Mol Sci. 2017; 18, 2628.Google Scholar
123. Martinez, SR, Ma, Q, Dasgupta, C, Meng, X, Zhang, L. MicroRNA-210 suppresses glucocorticoid receptor expression in response to hypoxia in fetal rat cardiomyocytes. Oncotarget. 2017; 8, 80249–80264.Google Scholar
124. Chan, YC, Banerjee, J, Choi, SY, Sen, CK. miR-210: the master hypoxamir. Microcirculation. 2012; 19, 215–223.Google Scholar
125. Huang, X, Zuo, J. Emerging roles of miR-210 and other non-coding RNAs in the hypoxic response. Acta Biochim Biophys Sin (Shanghai). 2014; 46, 220–232.Google Scholar
126. Guan, J, Long, K, Ma, J, et al. Comparative analysis of the microRNA transcriptome between yak and cattle provides insight into high-altitude adaptation. PeerJ. 2017; 5, e3959.Google Scholar
127. El Azzouzi, H, Leptidis, S, Dirkx, E, et al. The hypoxia-inducible microRNA cluster miR-199a approximately 214 targets myocardial PPARdelta and impairs mitochondrial fatty acid oxidation. Cell Metab. 2013; 18, 341–354.Google Scholar
128. Maloyan, A, Muralimanoharan, S, Huffman, S, et al. Identification and comparative analyses of myocardial miRNAs involved in the fetal response to maternal obesity. Physiol Genomics. 2013; 45, 889–900.Google Scholar
129. Kuwabara, Y, Horie, T, Baba, O, et al. MicroRNA-451 exacerbates lipotoxicity in cardiac myocytes and high-fat diet-induced cardiac hypertrophy in mice through suppression of the LKB1/AMPK pathway. Circ Res. 2015; 116, 279–288.Google Scholar
130. Guedes, EC, Franca, GS, Lino, CA, et al. MicroRNA expression signature is altered in the cardiac remodeling induced by high fat diets. J Cell Physiol. 2016; 231, 1771–1783.Google Scholar
131. Floris, I, Descamps, B, Vardeu, A, et al. Gestational diabetes mellitus impairs fetal endothelial cell functions through a mechanism involving microRNA-101 and histone methyltransferase enhancer of zester homolog-2. Arterioscler Thromb Vasc Biol. 2015; 35, 664–674.Google Scholar
132. Siddeek, B, Lakhdari, N, Inoubli, L, et al. Developmental epigenetic programming of adult germ cell death disease: polycomb protein EZH2-miR-101 pathway. Epigenomics. 2016; 8, 1459–1479.Google Scholar
133. Fernandez-Twinn, DS, Blackmore, HL, Siggens, L, et al. The programming of cardiac hypertrophy in the offspring by maternal obesity is associated with hyperinsulinemia, AKT, ERK, and mTOR activation. Endocrinology. 2012; 153, 5961–5971.Google Scholar
134. Wing-Lun, E, Eaton, SA, Hur, SS, et al. Nutrition has a pervasive impact on cardiac microRNA expression in isogenic mice. Epigenetics. 2016; 11, 475–481.Google Scholar
135. Grueter, CE, Van Rooij, E, Johnson, BA, et al. A cardiac microRNA governs systemic energy homeostasis by regulation of MED13. Cell. 2012; 149, 671–683.Google Scholar
136. Zhu, C, Yu, ZB, Zhu, JG, et al. Differential expression profile of MicroRNAs during differentiation of cardiomyocytes exposed to polychlorinated biphenyls. Int J Mol Sci. 2012; 13, 15955–15966.Google Scholar
137. Christopher, AF, Kaur, RP, Kaur, G, Kaur, A, Gupta, V, Bansal, P. MicroRNA therapeutics: discovering novel targets and developing specific therapy. Perspect Clin Res. 2016; 7, 68–74.Google Scholar
138. Rupaimoole, R, Slack, FJ. MicroRNA therapeutics: towards a new era for the management of cancer and other diseases. Nat Rev Drug Discov. 2017; 16, 203–222.Google Scholar
139. Montgomery, RL, Hullinger, TG, Semus, HM, et al. Therapeutic inhibition of miR-208a improves cardiac function and survival during heart failure. Circulation. 2011; 124, 1537–1547.Google Scholar
140. Rayner, KJ, Sheedy, FJ, Esau, CC, et al. Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis. J Clin Invest. 2011; 121, 2921–2931.Google Scholar
141. Zeng, XC, Li, L, Wen, H, Bi, Q. MicroRNA-128 inhibition attenuates myocardial ischemia/reperfusion injury-induced cardiomyocyte apoptosis by the targeted activation of peroxisome proliferator-activated receptor gamma. Mol Med Rep. 2016; 14, 129–136.Google Scholar
142. Jiang, C, Ji, N, Luo, G, et al. The effects and mechanism of miR-92a and miR-126 on myocardial apoptosis in mouse ischemia-reperfusion model. Cell Biochem Biophys. 2014; 70, 1901–1906.Google Scholar
143. Zhang, Y, Qin, W, Zhang, L, et al. MicroRNA-26a prevents endothelial cell apoptosis by directly targeting TRPC6 in the setting of atherosclerosis. Sci Rep. 2015; 5, 9401.Google Scholar
144. Hullinger, TG, Montgomery, RL, Seto, AG, et al. Inhibition of miR-15 protects against cardiac ischemic injury. Circ Res. 2012; 110, 71–81.Google Scholar
145. Bernardo, BC, Gao, XM, Winbanks, CE, et al. Therapeutic inhibition of the miR-34 family attenuates pathological cardiac remodeling and improves heart function. Proc Natl Acad Sci U S A. 2012; 109, 17615–17620.Google Scholar
146. Li, J, Li, Y, Jiao, J, et al. Mitofusin 1 is negatively regulated by microRNA 140 in cardiomyocyte apoptosis. Mol Cell Biol. 2014; 34, 1788–1799.Google Scholar
147. Bonci, D. MicroRNA-21 as therapeutic target in cancer and cardiovascular disease. Recent Pat Cardiovasc Drug Discov. 2010; 5, 156–161.Google Scholar
148. Wahlquist, C, Jeong, D, Rojas-Munoz, A, et al. Inhibition of miR-25 improves cardiac contractility in the failing heart. Nature. 2014; 508, 531–535.Google Scholar
149. Hu, S, Huang, M, Li, Z, et al. MicroRNA-210 as a novel therapy for treatment of ischemic heart disease. Circulation. 2010; 122(Suppl.), S124–S131.Google Scholar
150. Wang, Y, Zhang, L, Li, Y, et al. Exosomes/microvesicles from induced pluripotent stem cells deliver cardioprotective miRNAs and prevent cardiomyocyte apoptosis in the ischemic myocardium. Int J Cardiol. 2015; 192, 61–69.Google Scholar
151. Andrade, DC, Arce-Alvarez, A, Toledo, C, et al. Exercise training improve cardiac autonomic control, cardiac function and arrhythmogenesis in rats with preserved ejection fraction heart failure. J Appl Physiol (1985). 2017; 123, 567–577.Google Scholar
152. Denham, J, Prestes, PR. Muscle-enriched microRNAs isolated from whole blood are regulated by exercise and are potential biomarkers of cardiorespiratory fitness. Front Genet. 2016; 7, 196.Google Scholar
153. Zhao, Y, Ma, Z. Swimming training affects apoptosis-related microRNAs and reduces cardiac apoptosis in mice. Gen Physiol Biophys. 2016; 35, 443–450.Google Scholar
154. Lew, JK, Pearson, JT, Schwenke, DO, Katare, R. Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways. Cardiovasc Diabetol. 2017; 16, 10.Google Scholar
155. Melo, SF, Barauna, VG, Neves, VJ, et al. Exercise training restores the cardiac microRNA-1 and -214 levels regulating Ca2+ handling after myocardial infarction. BMC Cardiovasc Disord. 2015; 15, 166.Google Scholar
156. Barr, LA, Shimizu, Y, Lambert, JP, Nicholson, CK, Calvert, JW. Hydrogen sulfide attenuates high fat diet-induced cardiac dysfunction via the suppression of endoplasmic reticulum stress. Nitric Oxide. 2015; 46, 145–156.Google Scholar
157. Khatua, TN, Adela, R, Banerjee, SK. Garlic and cardioprotection: insights into the molecular mechanisms. Can J Physiol Pharmacol. 2013; 91, 448–458.Google Scholar
158. Jain, SK, Bull, R, Rains, JL, et al. Low levels of hydrogen sulfide in the blood of diabetes patients and streptozotocin-treated rats causes vascular inflammation? Antioxid Redox Signal. 2010; 12, 1333–1337.Google Scholar
159. Peh, MT, Anwar, AB, Ng, DS, Atan, MS, Kumar, SD, Moore, PK. Effect of feeding a high fat diet on hydrogen sulfide (H2S) metabolism in the mouse. Nitric Oxide. 2014; 41, 138–145.Google Scholar
160. Kesherwani, V, Nandi, SS, Sharawat, SK, Shahshahan, HR, Mishra, PK. Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes. Mol Cell Biochem. 2015; 404, 241–250.Google Scholar
161. Kang, B, Hong, J, Xiao, J, et al. Involvement of miR-1 in the protective effect of hydrogen sulfide against cardiomyocyte apoptosis induced by ischemia/reperfusion. Mol Biol Rep. 2014; 41, 6845–6853.Google Scholar
162. Gray, C, Li, M, Patel, R, Reynolds, CM, Vickers, MH. Let-7 miRNA profiles are associated with the reversal of left ventricular hypertrophy and hypertension in adult male offspring from mothers undernourished during pregnancy after preweaning growth hormone treatment. Endocrinology. 2014; 155, 4808–4817.Google Scholar
163. Li, N, Guenancia, C, Rigal, E, et al. Short-term moderate diet restriction in adulthood can reverse oxidative, cardiovascular and metabolic alterations induced by postnatal overfeeding in mice. Sci Rep. 2016; 6, 30817.Google Scholar
164. Sygitowicz, G, Tomaniak, M, Blaszczyk, O, Koltowski, L, Filipiak, KJ, Sitkiewicz, D. Circulating microribonucleic acids miR-1, miR-21 and miR-208a in patients with symptomatic heart failure: preliminary results. Arch Cardiovasc Dis. 2015; 108, 634–642.Google Scholar
165. Naga Prasad, SV, Gupta, MK, Duan, ZH, et al. A unique microRNA profile in end-stage heart failure indicates alterations in specific cardiovascular signaling networks. PloS One. 2017; 12, e0170456.Google Scholar
166. Su, X, Liang, H, Wang, H, et al. Over-expression of microRNA-1 causes arrhythmia by disturbing intracellular trafficking system. Sci Rep. 2017; 7, 46259.Google Scholar
167. Yang, B, Lin, H, Xiao, J, et al. The muscle-specific microRNA miR-1 regulates cardiac arrhythmogenic potential by targeting GJA1 and KCNJ2. Nat Med. 2007; 13, 486–491.Google Scholar
168. Navickas, R, Gal, D, Laucevicius, A, Taparauskaite, A, Zdanyte, M, Holvoet, P. Identifying circulating microRNAs as biomarkers of cardiovascular disease: a systematic review. Cardiovasc Res. 2016; 111, 322–337.Google Scholar
169. Liu, L, Yuan, Y, He, X, Xia, X, Mo, X. MicroRNA-1 upregulation promotes myocardiocyte proliferation and suppresses apoptosis during heart development. Mol Med Rep. 2017; 15, 2837–2842.Google Scholar
170. Jung, S, Bohan, A. Genome-wide sequencing and quantification of circulating microRNAs for dogs with congestive heart failure secondary to myxomatous mitral valve degeneration. Am J Vet Res. 2018; 79, 163–169.Google Scholar
171. Luo, S, Chen, Y, He, R, Shi, Y, Su, L. Rescuing infusion of miRNA-1 prevents cardiac remodeling in a heart-selective miRNA deficient mouse. Biochem Biophys Res Commun. 2018; 495, 607–613.Google Scholar
172. Tatsuguchi, M, Seok, HY, Callis, TE, et al. Expression of microRNAs is dynamically regulated during cardiomyocyte hypertrophy. J Mol Cell Cardiol. 2007; 42, 1137–1141.Google Scholar
173. Long, G, Wang, F, Duan, Q, et al. Human circulating microRNA-1 and microRNA-126 as potential novel indicators for acute myocardial infarction. Int J Biol Sci. 2012; 8, 811–818.Google Scholar
174. Cheng, Y, Tan, N, Yang, J, et al. A translational study of circulating cell-free microRNA-1 in acute myocardial infarction. Clin Sci. 2010; 119, 87–95.Google Scholar
175. Yang, VK, Tai, AK, Huh, TP, et al. Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease. PLoS One. 2018; 13, e0188617.Google Scholar
176. Marques, FZ, Vizi, D, Khammy, O, Mariani, JA, Kaye, DM. The transcardiac gradient of cardio-microRNAs in the failing heart. Eur J Heart Fail. 2016; 18, 1000–1008.Google Scholar
177. Faccini, J, Ruidavets, JB, Cordelier, P, et al. Circulating miR-155, miR-145 and let-7c as diagnostic biomarkers of the coronary artery disease. Sci Rep. 2017; 7, 42916.Google Scholar
178. Cao, L, Kong, LP, Yu, ZB, et al. microRNA expression profiling of the developing mouse heart. Int J Mol Med. 2012; 30, 1095–1104.Google Scholar
179. Wang, H, Shi, J, Li, B, Zhou, Q, Kong, X, Bei, Y. MicroRNA expression signature in human calcific aortic valve disease. Biomed Res Int. 2017; 2017, 4820275.Google Scholar
180. Wang, X, Wang, HX, Li, YL, et al. MicroRNA Let-7i negatively regulates cardiac inflammation and fibrosis. Hypertension. 2015; 66, 776–785.Google Scholar
181. Lu, Y, Hou, S, Huang, D, et al. Expression profile analysis of circulating microRNAs and their effects on ion channels in Chinese atrial fibrillation patients. Int J Clin Exp Med. 2015; 8, 845–853.Google Scholar
182. Wang, L, Ma, L, Fan, H, Yang, Z, Li, L, Wang, H. MicroRNA-9 regulates cardiac fibrosis by targeting PDGFR-beta in rats. J Physiol Biochem. 2016; 72, 213–223.Google Scholar
183. Wang, K, Long, B, Zhou, J, Li, PF. miR-9 and NFATc3 regulate myocardin in cardiac hypertrophy. J Biol Chem. 2010; 285, 11903–11912.Google Scholar
184. Jeyabal, P, Thandavarayan, RA, Joladarashi, D, et al. MicroRNA-9 inhibits hyperglycemia-induced pyroptosis in human ventricular cardiomyocytes by targeting ELAVL1. Biochem Biophys Res Commun. 2016; 471, 423–429.Google Scholar
185. Luo, L, Chen, B, Li, S, et al. Plasma miR-10a: a potential biomarker for coronary artery disease. Dis Markers. 2016; 2016, 3841927.Google Scholar
186. Chen, F, Zhao, X, Peng, J, Bo, L, Fan, B, Ma, D. Integrated microRNA-mRNA analysis of coronary artery disease. Mol Biol Rep. 2014; 41, 5505–5511.Google Scholar
187. Danielson, LS, Park, DS, Rotllan, N, et al. Cardiovascular dysregulation of miR-17-92 causes a lethal hypertrophic cardiomyopathy and arrhythmogenesis. FASEB J. 2013; 27, 1460–1467.Google Scholar
188. Liu, F, Li, R, Zhang, Y, Qiu, J, Ling, W. Association of plasma MiR-17-92 with dyslipidemia in patients with coronary artery disease. Medicine (Baltimore). 2014; 93, e98.Google Scholar
189. Bai, Y, Wang, J, Morikawa, Y, Bonilla-Claudio, M, Klysik, E, Martin, JF. Bmp signaling represses Vegfa to promote outflow tract cushion development. Development. 2013; 140, 3395–3402.Google Scholar
190. Ventura, A, Young, AG, Winslow, MM, et al. Targeted deletion reveals essential and overlapping functions of the miR-17 through 92 family of miRNA clusters. Cell. 2008; 132, 875–886.Google Scholar
191. Van Almen, GC, Verhesen, W, Van Leeuwen, RE, et al. MicroRNA-18 and microRNA-19 regulate CTGF and TSP-1 expression in age-related heart failure. Aging Cell. 2011; 10, 769–779.Google Scholar
192. Benz, A, Kossack, M, Auth, D, et al. miR-19b regulates ventricular action potential duration in zebrafish. Sci Rep. 2016; 6, 36033.Google Scholar
193. Zeller, T, Keller, T, Ojeda, F, et al. Assessment of microRNAs in patients with unstable angina pectoris. Eur Heart J. 2014; 35, 2106–2114.Google Scholar
194. Song, DW, Ryu, JY, Kim, JO, Kwon, EJ, Kim, DH. The miR-19a/b family positively regulates cardiomyocyte hypertrophy by targeting atrogin-1 and MuRF-1. Biochem J. 2014; 457, 151–162.Google Scholar
195. Zhong, J, He, Y, Chen, W, Shui, X, Chen, C, Lei, W. Circulating microRNA-19a as a potential novel biomarker for diagnosis of acute myocardial infarction. Int J Mol Sci. 2014; 15, 20355–20364.Google Scholar
196. Copier, CU, Leon, L, Fernandez, M, Contador, D, Calligaris, SD. Circulating miR-19b and miR-181b are potential biomarkers for diabetic cardiomyopathy. Sci Rep. 2017; 7, 13514.Google Scholar
197. Lin, J, Xue, A, Li, L, et al. MicroRNA-19b downregulates gap junction protein alpha1 and synergizes with microRNA-1 in viral myocarditis. Int J Mol Sci. 2016; 17, 741.Google Scholar
198. Xu, HF, Gao, XT, Lin, JY, et al. MicroRNA-20b suppresses the expression of ZFP-148 in viral myocarditis. Mol Cell Biochem. 2017; 429, 199–210.Google Scholar
199. Barana, A, Matamoros, M, Dolz-Gaiton, P, et al. Chronic atrial fibrillation increases microRNA-21 in human atrial myocytes decreasing L-type calcium current. Circ Arrhythm Electrophysiol. 2014; 7, 861–868.Google Scholar
200. Wang, F, Long, G, Zhao, C, et al. Atherosclerosis-related circulating miRNAs as novel and sensitive predictors for acute myocardial infarction. PLoS One. 2014; 9, e105734.Google Scholar
201. Kolpa, HJ, Peal, DS, Lynch, SN, et al. miR-21 represses Pdcd4 during cardiac valvulogenesis. Development. 2013; 140, 2172–2180.Google Scholar
202. Thum, T, Gross, C, Fiedler, J, et al. MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts. Nature. 2008; 456, 980–984.Google Scholar
203. Shen, E, Diao, X, Wang, X, Chen, R, Hu, B. MicroRNAs involved in the mitogen-activated protein kinase cascades pathway during glucose-induced cardiomyocyte hypertrophy. Am J Pathol. 2011; 179, 639–650.Google Scholar
204. Xu, HF, Ding, YJ, Zhang, ZX, et al. MicroRNA21 regulation of the progression of viral myocarditis to dilated cardiomyopathy. Mol Med Rep. 2014; 10, 161–168.Google Scholar
205. Corsten, MF, Papageorgiou, A, Verhesen, W, et al. MicroRNA profiling identifies microRNA-155 as an adverse mediator of cardiac injury and dysfunction during acute viral myocarditis. Circ Res. 2012; 111, 415–425.Google Scholar
206. Van Boven, N, Akkerhuis, KM, Anroedh, SS, et al. Serially measured circulating miR-22-3p is a biomarker for adverse clinical outcome in patients with chronic heart failure: the Bio-SHiFT study. Int J Cardiol. 2017; 235, 124–132.Google Scholar
207. Hong, Y, Cao, H, Wang, Q, et al. MiR-22 may suppress fibrogenesis by targeting TGFbetaR I in cardiac fibroblasts. Cell Physiol Biochem. 2016; 40, 1345–1353.Google Scholar
208. Maciejak, A, Kiliszek, M, Opolski, G, et al. miR-22-5p revealed as a potential biomarker involved in the acute phase of myocardial infarction via profiling of circulating microRNAs. Mol Med Rep. 2016; 14, 2867–2875.Google Scholar
209. Lagendijk, AK, Goumans, MJ, Burkhard, SB, Bakkers, J. MicroRNA-23 restricts cardiac valve formation by inhibiting Has2 and extracellular hyaluronic acid production. Circ Res. 2011; 109, 649–657.Google Scholar
210. Van Rooij, E, Sutherland, LB, Liu, N, et al. A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure. Proc Natl Acad Sci U S A. 2006; 103, 18255–18260.Google Scholar
211. Chen, Z, Lu, S, Xu, M, Liu, P, Ren, R, Ma, W. Role of miR-24, furin, and transforming growth factor-beta1 signal pathway in fibrosis after cardiac infarction. Med Sci Monit. 2017; 23, 65–70.Google Scholar
212. Dirkx, E, Gladka, MM, Philippen, LE, et al. Nfat and miR-25 cooperate to reactivate the transcription factor Hand2 in heart failure. Nat Cell Biol. 2013; 15, 1282–1293.Google Scholar
213. Luo, X, Pan, Z, Shan, H, et al. MicroRNA-26 governs profibrillatory inward-rectifier potassium current changes in atrial fibrillation. J Clin Invest. 2013; 123, 1939–1951.Google Scholar
214. Nigam, V, Sievers, HH, Jensen, BC, et al. Altered microRNAs in bicuspid aortic valve: a comparison between stenotic and insufficient valves. J Heart Valve Dis. 2010; 19, 459–465.Google Scholar
215. Xu, HX, Wang, Y, Zheng, DD, et al. Differential expression of microRNAs in calcific aortic stenosis. Clin Lab. 2017; 63, 1163–1170.Google Scholar
216. Wei, C, Kim, IK, Kumar, S, et al. NF-kappaB mediated miR-26a regulation in cardiac fibrosis. J Cell Physiol. 2013; 228, 1433–1442.Google Scholar
217. Han, M, Yang, Z, Sayed, D, et al. GATA4 expression is primarily regulated via a miR-26b-dependent post-transcriptional mechanism during cardiac hypertrophy. Cardiovasc Res. 2012; 93, 645–654.Google Scholar
218. Li, C, Chen, X, Huang, J, Sun, Q, Wang, L. Clinical impact of circulating miR-26a, miR-191, and miR-208b in plasma of patients with acute myocardial infarction. Eur J Med Res. 2015; 20, 58.Google Scholar
219. Takahashi, K, Sasano, T, Sugiyama, K, et al. High-fat diet increases vulnerability to atrial arrhythmia by conduction disturbance via miR-27b. J Mol Cell Cardiol. 2016; 90, 38–46.Google Scholar
220. Yu, K, Ji, Y, Wang, H, et al. Association of miR-196a2, miR-27a, and miR-499 polymorphisms with isolated congenital heart disease in a Chinese population. Genet Mol Res. 2016; 15, gmr15048929.Google Scholar
221. O’Brien, JE Jr., Kibiryeva, N, Zhou, XG, et al. Noncoding RNA expression in myocardium from infants with tetralogy of Fallot. Circ Cardiovasc Genet. 2012; 5, 279–286.Google Scholar
222. Wang, J, Song, Y, Zhang, Y, et al. Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice. Cell Res. 2012; 22, 516–527.Google Scholar
223. Wang, Y, Chen, S, Gao, Y, Zhang, S. Serum MicroRNA-27b as a screening biomarker for left ventricular hypertrophy. Tex Heart Inst J. 2017; 44, 385–389.Google Scholar
224. Zhu, S, Cao, L, Zhu, J, et al. Identification of maternal serum microRNAs as novel non-invasive biomarkers for prenatal detection of fetal congenital heart defects. Clin Chim Acta. 2013; 424, 66–72.Google Scholar
225. Shi, J, Liu, H, Wang, H, Kong, X. MicroRNA expression signature in degenerative aortic stenosis. Biomed Res Int. 2016; 2016, 4682172.Google Scholar
226. Van Rooij, E, Sutherland, LB, Thatcher, JE, et al. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis. Proc Natl Acad Sci U S A. 2008; 105, 13027–13032.Google Scholar
227. Sassi, Y, Avramopoulos, P, Ramanujam, D, et al. Cardiac myocyte miR-29 promotes pathological remodeling of the heart by activating Wnt signaling. Nat Commun. 2017; 8, 1614.Google Scholar
228. Li, H, Li, S, Yu, B, Liu, S. Expression of miR-133 and miR-30 in chronic atrial fibrillation in canines. Mol Med Rep. 2012; 5, 1457–1460.Google Scholar
229. Liu, X, Li, M, Peng, Y, et al. miR-30c regulates proliferation, apoptosis and differentiation via the Shh signaling pathway in P19 cells. Exp Mol Med. 2016; 48, e248.Google Scholar
230. Duisters, RF, Tijsen, AJ, Schroen, B, et al. miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remodeling. Circ Res. 2009; 104, 170–178, 176p following 178.Google Scholar
231. Pan, W, Zhong, Y, Cheng, C, et al. MiR-30-regulated autophagy mediates angiotensin II-induced myocardial hypertrophy. PLoS One. 2013; 8, e53950.Google Scholar
232. Meder, B, Keller, A, Vogel, B, et al. MicroRNA signatures in total peripheral blood as novel biomarkers for acute myocardial infarction. Basic Res Cardiol. 2011; 106, 13–23.Google Scholar
233. Zhang, X, Fernandez-Hernando, C. miR-33 regulation of adaptive fibrotic response in cardiac remodeling. Circ Res. 2017; 120, 753–755.Google Scholar
234. Gacon, J, Kablak-Ziembicka, A, Stepien, E, et al. Decision-making microRNAs (miR-124, -133a/b, -34a and -134) in patients with occluded target vessel in acute coronary syndrome. Kardiol Pol. 2016; 74, 280–288.Google Scholar
235. Boon, RA, Iekushi, K, Lechner, S, et al. MicroRNA-34a regulates cardiac ageing and function. Nature. 2013; 495, 107–110.Google Scholar
236. Huang, J, Sun, W, Huang, H, et al. miR-34a modulates angiotensin II-induced myocardial hypertrophy by direct inhibition of ATG9A expression and autophagic activity. PLoS One. 2014; 9, e94382.Google Scholar
237. Greco, S, Fasanaro, P, Castelvecchio, S, et al. MicroRNA dysregulation in diabetic ischemic heart failure patients. Diabetes. 2012; 61, 1633–1641.Google Scholar
238. Niculescu, LS, Simionescu, N, Sanda, GM, et al. MiR-486 and miR-92a identified in circulating HDL discriminate between stable and vulnerable coronary artery disease patients. PLoS One. 2015; 10, e0140958.Google Scholar
239. Taurino, C, Miller, WH, McBride, MW, et al. Gene expression profiling in whole blood of patients with coronary artery disease. Clin Sci (Lond). 2010; 119, 335–343.Google Scholar
240. Catalucci, D, Latronico, MV, Condorelli, G. MicroRNAs control gene expression: importance for cardiac development and pathophysiology. Ann N Y Acad Sci. 2008; 1123, 20–29.Google Scholar
241. JF, OS, Neylon, A, McGorrian, C, Blake, GJ. miRNA-93-5p and other miRNAs as predictors of coronary artery disease and STEMI. Int J Cardiol. 2016; 224, 310–316.Google Scholar
242. Li, Q, Freeman, LM, Rush, JE, Laflamme, DP. Expression profiling of circulating microRNAs in canine myxomatous mitral valve disease. Int J Mol Sci. 2015; 16, 14098–14108.Google Scholar
243. Yang, Y, Ago, T, Zhai, P, Abdellatif, M, Sadoshima, J. Thioredoxin 1 negatively regulates angiotensin II-induced cardiac hypertrophy through upregulation of miR-98/let-7. Circ Res. 2011; 108, 305–313.Google Scholar
244. Natsume, Y, Oaku, K, Takahashi, K, et al. Combined analysis of human and experimental murine samples identified novel circulating microRNAs as biomarkers for atrial fibrillation. Circ J. 2018; 82, 965–973.Google Scholar
245. Kehler, L, Biro, O, Lazar, L, Rigo, J Jr., Nagy, B. Elevated hsa-miR-99a levels in maternal plasma may indicate congenital heart defects. Biomed Rep. 2015; 3, 869–873.Google Scholar
246. Sucharov, C, Bristow, MR, Port, JD. miRNA expression in the failing human heart: functional correlates. J Mol Cell Cardiol. 2008; 45, 185–192.Google Scholar
247. Pan, Z, Sun, X, Shan, H, et al. MicroRNA-101 inhibited postinfarct cardiac fibrosis and improved left ventricular compliance via the FBJ osteosarcoma oncogene/transforming growth factor-beta1 pathway. Circulation. 2012; 126, 840–850.Google Scholar
248. Wei, L, Yuan, M, Zhou, R, et al. MicroRNA-101 inhibits rat cardiac hypertrophy by targeting Rab1a. J Cardiovasc Pharmacol. 2015; 65, 357–363.Google Scholar
249. Chiang, DY, Kongchan, N, Beavers, DL, et al. Loss of microRNA-106b-25 cluster promotes atrial fibrillation by enhancing ryanodine receptor type-2 expression and calcium release. Circ Arrhythm Electrophysiol. 2014; 7, 1214–1222.Google Scholar
250. Gao, W, He, HW, Wang, ZM, et al. Plasma levels of lipometabolism-related miR-122 and miR-370 are increased in patients with hyperlipidemia and associated with coronary artery disease. Lipids Health Dis. 2012; 11, 55.Google Scholar
251. Martinez-Micaelo, N, Beltran-Debon, R, Baiges, I, Faiges, M, Alegret, JM. Specific circulating microRNA signature of bicuspid aortic valve disease. J Transl Med. 2017; 15, 76.Google Scholar
252. Beaumont, J, Lopez, B, Hermida, N, et al. microRNA-122 down-regulation may play a role in severe myocardial fibrosis in human aortic stenosis through TGF-beta1 up-regulation. Clin Sci (Lond). 2014; 126, 497–506.Google Scholar
253. D’Alessandra, Y, Devanna, P, Limana, F, et al. Circulating microRNAs are new and sensitive biomarkers of myocardial infarction. Eur Heart J. 2010; 31, 2765–2773.Google Scholar
254. Kuhn, DE, Nuovo, GJ, Martin, MM, et al. Human chromosome 21-derived miRNAs are overexpressed in down syndrome brains and hearts. Biochem Biophys Res Commun. 2008; 370, 473–477.Google Scholar
255. Liu, H, Qin, H, Chen, GX, et al. Comparative expression profiles of microRNA in left and right atrial appendages from patients with rheumatic mitral valve disease exhibiting sinus rhythm or atrial fibrillation. J Transl Med. 2014; 12, 90.Google Scholar
256. Nagpal, V, Rai, R, Place, AT, et al. MiR-125b is critical for fibroblast-to-myofibroblast transition and cardiac fibrosis. Circulation. 2016; 133, 291–301.Google Scholar
257. Fukushima, Y, Nakanishi, M, Nonogi, H, Goto, Y, Iwai, N. Assessment of plasma miRNAs in congestive heart failure. Circ J. 2011; 75, 336–340.Google Scholar
258. Wang, X, Lian, Y, Wen, X, et al. Expression of miR-126 and its potential function in coronary artery disease. Afr Health Sci. 2017; 17, 474–480.Google Scholar
259. Zampetaki, A, Willeit, P, Tilling, L, et al. Prospective study on circulating MicroRNAs and risk of myocardial infarction. J Am Coll Cardiol. 2012; 60, 290–299.Google Scholar
260. Li, L, Bounds, KR, Chatterjee, P, Gupta, S. MicroRNA-130a, a potential antifibrotic target in cardiac fibrosis. J Am Heart Assoc. 2017; 6, e006763.Google Scholar
261. Qiao, G, Xia, D, Cheng, Z, Zhang, G. miR132 in atrial fibrillation directly targets connective tissue growth factor. Mol Med Rep. 2017; 16, 4143–4150.Google Scholar
262. Ucar, A, Gupta, SK, Fiedler, J, et al. The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy. Nat Commun. 2012; 3, 1078.Google Scholar
263. Wen, P, Song, D, Ye, H, et al. Circulating MiR-133a as a biomarker predicts cardiac hypertrophy in chronic hemodialysis patients. PLoS One. 2014; 9, e103079.Google Scholar
264. Belevych, AE, Sansom, SE, Terentyeva, R, et al. MicroRNA-1 and -133 increase arrhythmogenesis in heart failure by dissociating phosphatase activity from RyR2 complex. PLoS One. 2011; 6, e28324.Google Scholar
265. Liu, N, Bezprozvannaya, S, Williams, AH, et al. microRNA-133a regulates cardiomyocyte proliferation and suppresses smooth muscle gene expression in the heart. Genes Dev. 2008; 22, 3242–3254.Google Scholar
266. Care, A, Catalucci, D, Felicetti, F, et al. MicroRNA-133 controls cardiac hypertrophy. Nat Med. 2007; 13, 613–618.Google Scholar
267. He, F, Lv, P, Zhao, X, et al. Predictive value of circulating miR-328 and miR-134 for acute myocardial infarction. Mol Cell Biochem. 2014; 394, 137–144.Google Scholar
268. Yanagawa, B, Lovren, F, Pan, Y, et al. miRNA-141 is a novel regulator of BMP-2-mediated calcification in aortic stenosis. J Thorac Cardiovasc Surg. 2012; 144, 256–262.Google Scholar
269. Baseler, WA, Thapa, D, Jagannathan, R, Dabkowski, ER, Croston, TL, Hollander, JM. miR-141 as a regulator of the mitochondrial phosphate carrier (Slc25a3) in the type 1 diabetic heart. Am J Physiol Cell Physiol. 2012; 303, C1244–C1251.Google Scholar
270. Fichtlscherer, S, De Rosa, S, Fox, H, et al. Circulating microRNAs in patients with coronary artery disease. Circ Res. 2010; 107, 677–684.Google Scholar
271. Fernandes, T, Hashimoto, NY, Magalhaes, FC, et al. Aerobic exercise training-induced left ventricular hypertrophy involves regulatory MicroRNAs, decreased angiotensin-converting enzyme-angiotensin ii, and synergistic regulation of angiotensin-converting enzyme 2-angiotensin (1-7). Hypertension. 2011; 58, 182–189.Google Scholar
272. Yu, M, Liu, Y, Zhang, B, Shi, Y, Cui, L, Zhao, X. Inhibiting microRNA-144 abates oxidative stress and reduces apoptosis in hearts of streptozotocin-induced diabetic mice. Cardiovasc Pathol. 2015; 24, 375–381.Google Scholar
273. Cha, MJ, Jang, JK, Ham, O, et al. MicroRNA-145 suppresses ROS-induced Ca2+ overload of cardiomyocytes by targeting CaMKIIdelta. Biochem Biophys Res Commun. 2013; 435, 720–726.Google Scholar
274. Li, R, Yan, G, Zhang, Q, et al. miR-145 inhibits isoproterenol-induced cardiomyocyte hypertrophy by targeting the expression and localization of GATA6. FEBS Lett. 2013; 587, 1754–1761.Google Scholar
275. Van de Vrie, M, Heymans, S, Schroen, B. MicroRNA involvement in immune activation during heart failure. Cardiovasc Drugs Ther. 2011; 25, 161–170.Google Scholar
276. Liu, Z, Zhou, C, Liu, Y, et al. The expression levels of plasma micoRNAs in atrial fibrillation patients. PLoS One. 2012; 7, e44906.Google Scholar
277. Oerlemans, MI, Mosterd, A, Dekker, MS, et al. Early assessment of acute coronary syndromes in the emergency department: the potential diagnostic value of circulating microRNAs. EMBO Mol Med. 2012; 4, 1176–1185.Google Scholar
278. Huang, W, Tian, SS, Hang, PZ, Sun, C, Guo, J, Du, ZM. Combination of microRNA-21 and microRNA-146a attenuates cardiac dysfunction and apoptosis during acute myocardial infarction in mice. Mol Ther Nucleic Acids. 2016; 5, e296.Google Scholar
279. Patel, V, Carrion, K, Hollands, A, et al. The stretch responsive microRNA miR-148a-3p is a novel repressor of IKBKB, NF-kappaB signaling, and inflammatory gene expression in human aortic valve cells. FASEB J. 2015; 29, 1859–1868.Google Scholar
280. Bao, JL, Lin, L. MiR-155 and miR-148a reduce cardiac injury by inhibiting NF-kappaB pathway during acute viral myocarditis. Eur Rev Med Pharmacol Sci. 2014; 18, 2349–2356.Google Scholar
281. Ali Sheikh, MS, Xia, K, Li, F, et al. Circulating miR-765 and miR-149: potential noninvasive diagnostic biomarkers for geriatric coronary artery disease patients. Biomed Res Int. 2015; 2015, 740301.Google Scholar
282. Sayed, AS, Xia, K, Li, F, et al. The diagnostic value of circulating microRNAs for middle-aged (40-60-year-old) coronary artery disease patients. Clinics (Sao Paulo). 2015; 70, 257–263.Google Scholar
283. Liu, W, Liu, Y, Zhang, Y, et al. MicroRNA-150 protects against pressure overload-induced cardiac hypertrophy. J Cell Biochem. 2015; 116, 2166–2176.Google Scholar
284. Zhang, R, Lan, C, Pei, H, Duan, G, Huang, L, Li, L. Expression of circulating miR-486 and miR-150 in patients with acute myocardial infarction. BMC Cardiovasc Disord. 2015; 15, 51.Google Scholar
285. Zhang, D, Cui, Y, Li, B, Luo, X, Li, B, Tang, Y. miR-155 regulates high glucose-induced cardiac fibrosis via the TGF-beta signaling pathway. Mol Biosyst. 2016; 13, 215–224.Google Scholar
286. Seok, HY, Chen, J, Kataoka, M, et al. Loss of microRNA-155 protects the heart from pathological cardiac hypertrophy. Circ Res. 2014; 114, 1585–1595.Google Scholar
287. Li, J, Cao, Y, Ma, XJ, et al. Roles of miR-1-1 and miR-181c in ventricular septal defects. Int J Cardiol. 2013; 168, 1441–1446.Google Scholar
288. Zhu, J, Yao, K, Wang, Q, et al. Circulating miR-181a as a potential novel biomarker for diagnosis of acute myocardial infarction. Cell Physiol Biochem. 2016; 40, 1591–1602.Google Scholar
289. Kim, JO, Song, DW, Kwon, EJ, et al. miR-185 plays an anti-hypertrophic role in the heart via multiple targets in the calcium-signaling pathways. PLoS One. 2015; 10, e0122509.Google Scholar
290. Wang, K, Liu, CY, Zhou, LY, et al. APF lncRNA regulates autophagy and myocardial infarction by targeting miR-188-3p. Nat Commun. 2015; 6, 6779.Google Scholar
291. Wong, LL, Armugam, A, Sepramaniam, S, et al. Circulating microRNAs in heart failure with reduced and preserved left ventricular ejection fraction. Eur J Heart Fail. 2015; 17, 393–404.Google Scholar
292. Hang, P, Sun, C, Guo, J, Zhao, J, Du, Z. BDNF-mediates down-regulation of microRNA-195 inhibits ischemic cardiac apoptosis in rats. Int J Biol Sci. 2016; 12, 979–989.Google Scholar
293. Zheng, D, Ma, J, Yu, Y, et al. Silencing of miR-195 reduces diabetic cardiomyopathy in C57BL/6 mice. Diabetologia. 2015; 58, 1949–1958.Google Scholar
294. Schulte, C, Molz, S, Appelbaum, S, et al. miRNA-197 and miRNA-223 predict cardiovascular death in a cohort of patients with symptomatic coronary artery disease. PLoS One. 2015; 10, e0145930.Google Scholar
295. Li, Z, Song, Y, Liu, L, et al. miR-199a impairs autophagy and induces cardiac hypertrophy through mTOR activation. Cell Death Differ. 2017; 24, 1205–1213.Google Scholar
296. Lesizza, P, Prosdocimo, G, Martinelli, V, Sinagra, G, Zacchigna, S, Giacca, M. Single-dose intracardiac injection of pro-regenerative microRNAs improves cardiac function after myocardial infarction. Circ Res. 2017; 120, 1298–1304.Google Scholar
297. Vogel, B, Keller, A, Frese, KS, et al. Multivariate miRNA signatures as biomarkers for non-ischaemic systolic heart failure. Eur Heart J. 2013; 34, 2812–2822.Google Scholar
298. Feng, B, Cao, Y, Chen, S, Chu, X, Chu, Y, Chakrabarti, S. miR-200b mediates endothelial-to-mesenchymal transition in diabetic cardiomyopathy. Diabetes. 2016; 65, 768–779.Google Scholar
299. Chen, YT, Wang, J, Wee, AS, et al. Differential microRNA expression profile in myxomatous mitral valve prolapse and fibroelastic deficiency valves. Int J Mol Sci. 2016; 17, 753.Google Scholar
300. Song, R, Fullerton, DA, Ao, L, et al. Altered microRNA expression is responsible for the pro-osteogenic phenotype of interstitial cells in calcified human aortic valves. J Am Heart Assoc. 2017; 6, e005364.Google Scholar
301. Zhang, Y, Zheng, S, Geng, Y, et al. MicroRNA profiling of atrial fibrillation in canines: miR-206 modulates intrinsic cardiac autonomic nerve remodeling by regulating SOD1. PLoS One. 2015; 10, e0122674.Google Scholar
302. Wang, M, Ji, Y, Cai, S, Ding, W. MiR-206 suppresses the progression of coronary artery disease by modulating vascular endothelial growth factor (VEGF) expression. Med Sci Monit. 2016; 22, 5011–5020.Google Scholar
303. Limana, F, Esposito, G, D’Arcangelo, D, et al. HMGB1 attenuates cardiac remodelling in the failing heart via enhanced cardiac regeneration and miR-206-mediated inhibition of TIMP-3. PLoS One. 2011; 6, e19845.Google Scholar
304. Yang, Y, Del, Re DP, Nakano, N, et al. miR-206 mediates YAP-induced cardiac hypertrophy and survival. Circ Res. 2015; 117, 891–904.Google Scholar
305. Shan, ZX, Lin, QX, Deng, CY, et al. miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes. FEBS Lett. 2010; 584, 3592–3600.Google Scholar
306. Callis, TE, Pandya, K, Seok, HY, et al. MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. J Clin Invest. 2009; 119, 2772–2786.Google Scholar
307. Liu, H, Yang, N, Fei, Z, et al. Analysis of plasma miR-208a and miR-370 expression levels for early diagnosis of coronary artery disease. Biomed Rep. 2016; 5, 332–336.Google Scholar
308. Wang, BW, Wu, GJ, Cheng, WP, Shyu, KG. MicroRNA-208a increases myocardial fibrosis via endoglin in volume overloading heart. PLoS One. 2014; 9, e84188.Google Scholar
309. Ji, X, Takahashi, R, Hiura, Y, Hirokawa, G, Fukushima, Y, Iwai, N. Plasma miR-208 as a biomarker of myocardial injury. Clin Chem. 2009; 55, 1944–1949.Google Scholar
310. Corsten, MF, Dennert, R, Jochems, S, et al. Circulating MicroRNA-208b and MicroRNA-499 reflect myocardial damage in cardiovascular disease. Circ Cardiovasc Genet. 2010; 3, 499–506.Google Scholar
311. Arif, M, Pandey, R, Alam, P, et al. MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents. J Mol Med (Berl). 2017; 95, 1369–1385.Google Scholar
312. Xiao, J, Liang, D, Zhang, Y, et al. MicroRNA expression signature in atrial fibrillation with mitral stenosis. Physiol Genomics. 2011; 43, 655–664.Google Scholar
313. Dong, H, Dong, S, Zhang, L, et al. MicroRNA-214 exerts a Cardio-protective effect by inhibition of fibrosis. Anat Rec (Hoboken). 2016; 299, 1348–1357.Google Scholar
314. Yang, X, Qin, Y, Shao, S, et al. MicroRNA-214 inhibits left ventricular remodeling in an acute myocardial infarction rat model by suppressing cellular apoptosis via the phosphatase and tensin homolog (PTEN). Int Heart J. 2016; 57, 247–250.Google Scholar
315. Minami, Y, Satoh, M, Maesawa, C, et al. Effect of atorvastatin on microRNA 221/222 expression in endothelial progenitor cells obtained from patients with coronary artery disease. Eur J Clin Invest. 2009; 39, 359–367.Google Scholar
316. Verjans, R, Peters, T, Beaumont, FJ, et al. MicroRNA-221/222 family counteracts myocardial fibrosis in pressure overload-induced heart failure. Hypertension. 2018; 71, 280–288.Google Scholar
317. Coskunpinar, E, Cakmak, HA, Kalkan, AK, Tiryakioglu, NO, Erturk, M, Ongen, Z. Circulating miR-221-3p as a novel marker for early prediction of acute myocardial infarction. Gene. 2016; 591, 90–96.Google Scholar
318. Corsten, M, Heggermont, W, Papageorgiou, AP, et al. The microRNA-221/-222 cluster balances the antiviral and inflammatory response in viral myocarditis. Eur Heart J. 2015; 36, 2909–2919.Google Scholar
319. Li, D, Ji, L, Liu, L, et al. Characterization of circulating microRNA expression in patients with a ventricular septal defect. PLoS One. 2014; 9, e106318.Google Scholar
320. Song, CL, Liu, B, Diao, HY, et al. Down-regulation of microRNA-320 suppresses cardiomyocyte apoptosis and protects against myocardial ischemia and reperfusion injury by targeting IGF-1. Oncotarget. 2016; 7, 39740–39757.Google Scholar
321. Lu, Y, Zhang, Y, Wang, N, et al. MicroRNA-328 contributes to adverse electrical remodeling in atrial fibrillation. Circulation. 2010; 122, 2378–2387.Google Scholar
322. Du, W, Liang, H, Gao, X, et al. MicroRNA-328, a potential anti-fibrotic target in cardiac interstitial fibrosis. Cell Physiol Biochem. 2016; 39, 827–836.Google Scholar
323. Li, C, Li, X, Gao, X, et al. MicroRNA-328 as a regulator of cardiac hypertrophy. Int J Cardiol. 2014; 173, 268–276.Google Scholar
324. Ge, Y, Pan, S, Guan, D, et al. MicroRNA-350 induces pathological heart hypertrophy by repressing both p38 and JNK pathways. Biochim Biophys Acta. 2013; 1832, 1–10.Google Scholar
325. Garikipati, VN, Krishnamurthy, P, Verma, SK, et al. Negative regulation of miR-375 by interleukin-10 enhances bone marrow-derived progenitor cell-mediated myocardial repair and function after myocardial infarction. Stem Cells. 2015; 33, 3519–3529.Google Scholar
326. Ganesan, J, Ramanujam, D, Sassi, Y, et al. MiR-378 controls cardiac hypertrophy by combined repression of mitogen-activated protein kinase pathway factors. Circulation. 2013; 127, 2097–2106.Google Scholar
327. Yang, VK, Loughran, KA, Meola, DM, et al. Circulating exosome microRNA associated with heart failure secondary to myxomatous mitral valve disease in a naturally occurring canine model. J Extracell Vesicles. 2017; 6, 1350088.Google Scholar
328. Liu, T, Zhong, S, Rao, F, Xue, Y, Qi, Z, Wu, S. Catheter ablation restores decreased plasma miR-409-3p and miR-432 in atrial fibrillation patients. Europace. 2016; 18, 92–99.Google Scholar
329. Tijsen, AJ, Creemers, EE, Moerland, PD, et al. MiR423-5p as a circulating biomarker for heart failure. Circ Res. 2010; 106, 1035–1039.Google Scholar
330. Ren, J, Zhang, J, Xu, N, et al. Signature of circulating microRNAs as potential biomarkers in vulnerable coronary artery disease. PLoS One. 2013; 8, e80738.Google Scholar
331. Song, L, Su, M, Wang, S, et al. MiR-451 is decreased in hypertrophic cardiomyopathy and regulates autophagy by targeting TSC1. J Cell Mol Med. 2014; 18, 2266–2274.Google Scholar
332. Xu, X, Li, H. Integrated microRNAgene analysis of coronary artery disease based on miRNA and gene expression profiles. Mol Med Rep. 2016; 13, 3063–3073.Google Scholar
333. Liu, H, Chen, GX, Liang, MY, et al. Atrial fibrillation alters the microRNA expression profiles of the left atria of patients with mitral stenosis. BMC Cardiovasc Disord. 2014; 14, 10.Google Scholar
334. Harling, L, Lambert, J, Ashrafian, H, Darzi, A, Gooderham, NJ, Athanasiou, T. Elevated serum microRNA 483-5p levels may predict patients at risk of post-operative atrial fibrillation. Eur J Cardiothorac Surg. 2017; 51, 73–78.Google Scholar
335. Qiao, Y, Zhao, Y, Liu, Y, et al. miR-483-3p regulates hyperglycaemia-induced cardiomyocyte apoptosis in transgenic mice. Biochem Biophys Res Commun. 2016; 477, 541–547.Google Scholar
336. Wang, X, Zhang, X, Ren, XP, et al. MicroRNA-494 targeting both proapoptotic and antiapoptotic proteins protects against ischemia/reperfusion-induced cardiac injury. Circulation. 2010; 122, 1308–1318.Google Scholar
337. Ling, TY, Wang, XL, Chai, Q, et al. Regulation of the SK3 channel by microRNA-499--potential role in atrial fibrillation. Heart Rhythm. 2013; 10, 1001–1009.Google Scholar
338. Adachi, T, Nakanishi, M, Otsuka, Y, et al. Plasma microRNA 499 as a biomarker of acute myocardial infarction. Clin Chem. 2010; 56, 1183–1185.Google Scholar
339. Zhou, J, Shao, G, Chen, X, et al. miRNA 206 and miRNA 574-5p are highly expression in coronary artery disease. Biosci Rep. 2015; 36, e00295.Google Scholar
340. Weber, M, Baker, MB, Patel, RS, Quyyumi, AA, Bao, G, Searles, CD. MicroRNA expression profile in CAD patients and the impact of ACEI/ARB. Cardiol Res Pract. 2011; 2011, 532915.Google Scholar
341. Shan, H, Zhang, Y, Lu, Y, et al. Downregulation of miR-133 and miR-590 contributes to nicotine-induced atrial remodelling in canines. Cardiovasc Res. 2009; 83, 465–472.Google Scholar
342. Zhang, JS, Zhao, Y, Lv, Y, et al. miR-873 suppresses H9C2 cardiomyocyte proliferation by targeting GLI1. Gene. 2017; 626, 426–432.Google Scholar
343. Wang, K, Liu, F, Liu, CY, et al. The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873. Cell Death Differ. 2016; 23, 1394–1405.Google Scholar
344. Liang, D, Xu, X, Deng, F, et al. miRNA-940 reduction contributes to human tetralogy of Fallot development. J Cell Mol Med. 2014; 18, 1830–1839.Google Scholar
345. Wang, K, Long, B, Li, N, et al. MicroRNA-2861 regulates programmed necrosis in cardiomyocyte by impairing adenine nucleotide translocase 1 expression. Free Radic Biol Med. 2016; 91, 58–67.Google Scholar