Role of mitochondria in apoptosis

Exp Physiol. 2003 Jan;88(1):85-90. doi: 10.1113/eph8802503.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Caspases / physiology
  • Humans
  • Intracellular Membranes / physiology
  • Membrane Proteins / physiology*
  • Mitochondria / metabolism
  • Mitochondria / physiology*
  • Mitochondrial Proteins / physiology*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / physiology*
  • Signal Transduction / physiology*


  • Membrane Proteins
  • Mitochondrial Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Caspases