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线粒体通透性转换在心肌病中的作用。

Role of the mitochondrial permeability transition in myocardial disease.

作者信息

Weiss James N, Korge Paavo, Honda Henry M, Ping Peipei

机构信息

Cardiovascular Research Laboratory, Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, Los Angeles, Calif 90095-1760, USA.

出版信息

Circ Res. 2003 Aug 22;93(4):292-301. doi: 10.1161/01.RES.0000087542.26971.D4.

Abstract

Mitochondria play a key role in determining cell fate during exposure to stress. Their role during ischemia/reperfusion is particularly critical because of the conditions that promote both apoptosis by the mitochondrial pathway and necrosis by irreversible damage to mitochondria in association with mitochondrial permeability transition (MPT). MPT is caused by the opening of permeability transition pores in the inner mitochondrial membrane, leading to matrix swelling, outer membrane rupture, release of apoptotic signaling molecules such as cytochrome c from the intermembrane space, and irreversible injury to the mitochondria. During ischemia (the MPT priming phase), factors such as intracellular Ca2+ accumulation, long-chain fatty acid accumulation, and reactive oxygen species progressively increase mitochondrial susceptibility to MPT, increasing the likelihood that MPT will occur on reperfusion (the MPT trigger phase). Because functional cardiac recovery ultimately depends on mitochondrial recovery, cardioprotection by ischemic and pharmacological preconditioning must ultimately involve the prevention of MPT. Investigations into this area are beginning to unravel some of the mechanistic links between cardioprotective signaling and mitochondria.

摘要

线粒体在应激状态下决定细胞命运的过程中起着关键作用。由于缺血/再灌注期间的一些状况,其作用尤为关键,这些状况既会通过线粒体途径促进细胞凋亡,又会因线粒体通透性转换(MPT)导致线粒体发生不可逆损伤进而引发坏死。MPT是由线粒体内膜通透性转换孔的开放引起的,会导致线粒体基质肿胀、外膜破裂、凋亡信号分子(如细胞色素c)从膜间隙释放,以及线粒体的不可逆损伤。在缺血期间(MPT启动阶段),诸如细胞内Ca2+积累、长链脂肪酸积累和活性氧等因素会逐渐增加线粒体对MPT的易感性,从而增加再灌注时(MPT触发阶段)发生MPT的可能性。由于心脏功能的最终恢复取决于线粒体的恢复,缺血预处理和药物预处理所带来的心脏保护作用最终必定涉及对MPT的预防。对该领域的研究正开始揭示心脏保护信号与线粒体之间一些机制上的联系。

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