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Mitochondrial Dysfunction and Myocardial Ischemia-Reperfusion: Implications for Novel Therapies
Annual Review of Pharmacology and Toxicology ( IF 11.2 ) Pub Date : 2017-01-06 00:00:00 , DOI: 10.1146/annurev-pharmtox-010715-103335
Edward J Lesnefsky 1, 2 , Qun Chen 1 , Bernard Tandler 3 , Charles L Hoppel 4, 5, 6
Affiliation  

Mitochondria have emerged as key participants in and regulators of myocardial injury during ischemia and reperfusion. This review examines the sites of damage to cardiac mitochondria during ischemia and focuses on the impact of these defects. The concept that mitochondrial damage during ischemia leads to cardiac injury during reperfusion is addressed. The mechanisms that translate ischemic mitochondrial injury into cellular damage, during both ischemia and early reperfusion, are examined. Next, we discuss strategies that modulate and counteract these mechanisms of mitochondrial-driven injury. The new concept that mitochondria are not merely stochastic sites of oxidative and calcium-mediated injury but that they activate cellular responses of mitochondrial remodeling and cellular reactions that modulate the balance between cell death and recovery is reviewed, and the therapeutic implications of this concept are discussed.

中文翻译:



线粒体功能障碍和心肌缺血再灌注:对新疗法的影响



线粒体已成为缺血和再灌注期间心肌损伤的关键参与者和调节者。这篇综述检查了缺血期间心脏线粒体受损的部位,并重点关注这些缺陷的影响。解决了缺血期间线粒体损伤导致再灌注期间心脏损伤的概念。研究了在缺血和早期再灌注期间将缺血性线粒体损伤转化为细胞损伤的机制。接下来,我们讨论调节和抵消这些线粒体驱动损伤机制的策略。回顾了线粒体不仅是氧化和钙介导损伤的随机位点,而且还激活线粒体重塑的细胞反应和调节细胞死亡与恢复之间平衡的细胞反应的新概念,并讨论了该概念的治疗意义。

更新日期:2017-01-06
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