Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 78, Issue -, Pages 100-106Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2014.09.023
Keywords
Mitochondria; Permeability transition pore; Ischemia-reperfusion injury
Categories
Funding
- AIRC [IG13392]
- Telethon [GGP11082, GPP10005A]
- Ministero dell'Istruzione, dell'Universita e della Ricerca [FIRB RBAP11S8C3, 20107Z8XBW]
- NIH-PHS [R01GM069883, R03DA033978-01]
- University of Padova
- Fondazione Cassa di Risparmio di Padova e Rovigo
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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 (PIP), a high conductance channel that is critically regulated by a variety of pathophysiological effectors. Very recent work indicates that the PTP forms from the FATP 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. (C) 2014 The Authors. Published by Elsevier Ltd.
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