title: Mitochondrial permeability transition pore and calcium handling.
abstract: Opening of a large conductance channel in the inner mitochondrial membrane, known as the mitochondrial permeability transition (MPT) pore, has been shown to be a primary mediator of cell death in the heart subjected to ischemia-reperfusion injury. Inhibitors of the MPT have been shown to reduce cardiac ischemia-reperfusion injury. Furthermore, most cardioprotective strategies appear to reduce ischemic cell death either by reducing the triggers for the opening of the MPT, such as reducing calcium overload or reactive oxygen species, or by more direct inhibition of the MPT. This chapter focuses on key issues in the study of the MPT and provides some methods for measuring MPT opening in isolated mitochondria.
authors: Cardiac Physiology Section, Systems Biology Center, NHLBI, NIH, Bethesda, MD 20892, USA.
authors: Renee
authors: R
authors: Wong
authors: Charles
authors: C
authors: Steenbergen
authors: Elizabeth
authors: E
authors: Murphy
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D008929:Mitochondria, Heart / Q000378:metabolism*; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism*; D000083162:Mitochondrial Permeability Transition Pore; D008933:Mitochondrial Swelling; D051381:Rats
chemical_list: D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D002118:Calcium