Pathophysiology of mitochondrial cell death control

Cell Mol Life Sci. 1999 Dec;56(11-12):971-6. doi: 10.1007/s000180050486.


Mitochondria have been recently recognized to play a major role in the control of apoptosis or programmed cell death. Permeabilization of mitochondrial membranes, a decisive feature of early cell death, is regulated by members of the Bcl-2 family which interact with the permeability transition pore complex (PTPC). Thus, the cytoprotective oncoprotein Bcl-2 stabilizes the mitochondrial membrane barrier function, whereas the tumor suppressor protein Bax permeabilizes mitochondrial membranes. The regulation of membrane permeabilization is intertwined with that of the bioenergetic and redox functions of mitochondria. The implications of alterations in the composition of the PTPC and in mitochondrial function for the pathophysiology of cancer (reduced apoptosis) and neurodegeneration (enhanced apoptosis) are discussed.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis*
  • Humans
  • Intracellular Membranes / metabolism
  • Ion Channels*
  • Membrane Proteins / metabolism
  • Mitochondria / metabolism*
  • Mitochondria / pathology*
  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Permeability Transition Pore
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Neurodegenerative Diseases / metabolism
  • Neurodegenerative Diseases / pathology
  • Permeability
  • Solubility


  • Ion Channels
  • Membrane Proteins
  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Permeability Transition Pore