Pathophysiology of mitochondrial cell death control.

Abstract

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.

• Authors: H L Vieira, G Kroemer
• Journal: Cellular and molecular life sciences : CMLS (Cell Mol Life Sci) Vol. 56 Issue 11-12 Pg. 971-6 (Dec 1999) ISSN: 1420-682X [Print] Switzerland
• PMID: 11212328 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

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

Topics

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