The molecular composition of the mitochondrial permeability transition pore.
Uncontrolled cell death is a fundamental cause of organ disease in humans. However, despite the need for us to delineate the molecular machinery that underlies cardiomyocyte death, our knowledge of these lethal cellular processes is still limited. The discovery that mitochondrial dysfunction, and in particular the mitochondrial permeability transition (MPT) pore, is often a common cause of the cardiac cell mortality that underlies numerous cardiac diseases has been a first crucial step. The purpose of this review is to outline our current understanding of the molecular identity of the MPT pore and the many questions that still need to be answered.
Baines
Christopher P
CP
Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, Missouri 65211, USA. bainesc@missouri.edu
D000818:Animals; D006801:Humans; D000226:Mitochondrial ADP, ATP Translocases / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000737:chemistry / Q000378:metabolism*; D000083162:Mitochondrial Permeability Transition Pore; D008954:Models, Biological; D050994:Voltage-Dependent Anion Channels / Q000378:metabolism
D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D050994:Voltage-Dependent Anion Channels; D000226:Mitochondrial ADP, ATP Translocases