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The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection

Paolo BernardiDepartment of Biomedical Sciences, University of Padova, 35121 Padova, Italy; Consiglio Nazionale delle Ricerche Neuroscience Institute, University of Padova, 35121 Padova, Italy. Electronic address: [email protected]Fabio Di LisaDepartment of Biomedical Sciences, University of Padova, 35121 Padova, Italy; Consiglio Nazionale delle Ricerche Neuroscience Institute, University of Padova, 35121 Padova, Italy. Electronic address: [email protected]
2014en
ABI

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The mitochondrial permeability transition (PT) - an abrupt increase permeability of the inner membrane to solutes - is a causative event in ischemia-reperfusion injury of the heart, and the focus of intense research in cardioprotection. The PT is due to opening of the PT pore (PTP), a high conductance channel that is critically regulated by a variety of pathophysiological effectors. Very recent work indicates that the PTP forms from the F-ATP synthase, which would switch from an energy-conserving to an energy-dissipating device. This review provides an update on the current debate on how this transition is achieved, and on the PTP as a target for therapeutic intervention. This article is part of a Special Issue entitled "Mitochondria: from basic mitochondrial biology to cardiovascular disease".

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