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Role of mitochondria in apoptosis

Published online by Cambridge University Press:  09 January 2003

Erich Gulbins ,
Stephan Dreschers  and
Jürgen Bock
Erich Gulbins
Affiliation:
Department of Molecular Biology, University of Essen, Hufelandstraße 55, 45122 Essen, Germany
Stephan Dreschers
Affiliation:
Department of Molecular Biology, University of Essen, Hufelandstraße 55, 45122 Essen, Germany
Jürgen Bock
Affiliation:
Department of Molecular Biology, University of Essen, Hufelandstraße 55, 45122 Essen, Germany
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Abstract

Apoptosis is an evolutionary-conserved physiological mechanism to remove cells from an organism. Cellular apoptosis is mediated via an intracellular signalling programme that involves a variety of signalling molecules and cellular organelles including caspases, sphingomyelinases, Bcl-2-like proteins and proteins to cleave the DNA and mitochondria. Mitochondria contain several pro-apoptotic molecules that activate cytosolic proteins to execute apoptosis, block anti-apoptotic proteins in the cytosol and directly cleave nuclear DNA. Mitochondria trap these pro-apoptotic proteins and physically separate pro-apoptotic proteins from their cytoplasmic targets. Apoptosis is then initiated by the release of mitochondrial pro-apoptotic proteins into the cytosol. This process seems to be regulated by Bcl-2-like proteins and several ion channels, in particular the permeability transition pore (PTP) that is activated by almost all pro-apoptotic stimuli. Experimental Physiology (2003) 88.1, 85-90.

Type
Special Review Series - Biogenesis and Physiological Adaptation of Mitochondria
Information
Experimental Physiology , Volume 88 , Issue 1 , January 2003 , pp. 85 - 90
Copyright
© The Physiological Society 2003

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