Mitochondria "THE" target of myocardial conditioning

被引：74

作者：

Boengler, Kerstin ^{[1
]}

Lochnit, Guenter ^{[2
]}

Schulz, Rainer ^{[1
]}

机构：

[1] Justus Liebig Univ, Inst Physiol, Giessen, Germany

[2] Justus Liebig Univ, Inst Biochem, Giessen, Germany

来源：

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2018年 / 315卷 / 05期

关键词：

cardioprotection; conditioning; connexin43; ischemia-reperfusion; mitochondria; mitochondrial dynamics; mitochondrial permeability transition pore; reactive oxygen species; ISCHEMIA-REPERFUSION INJURY; PERMEABILITY TRANSITION PORE; COMPLEX-I ACTIVITY; NITRIC-OXIDE SYNTHASE; SHOCK-PROTEIN; 90; PRECONDITIONING PRESERVES; RAT-HEART; ELECTRON-TRANSPORT; INTERFIBRILLAR MITOCHONDRIA; CARDIAC MITOCHONDRIA;

D O I：

10.1152/ajpheart.00124.2018

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Several interventions, such as ischemic preconditioning, remote pre/perconditioning, or postconditioning, are known to decrease lethal myocardial ischemia-reperfusion injury. While several signal transduction pathways become activated by such maneuvers, they all have a common end point, namely, the mitochondria. These organelles represent an essential target of the cardioprotective strategies, and the preservation of mitochondrial function is central for the reduction of ischemia-reperfusion injury. In the present review, we address the role of mitochondria in the different conditioning strategies; in particular, we focus on alterations of mitochondrial function in terms of energy production, formation of reactive oxygen species, opening of the mitochondrial permeability transition pore, and mitochondrial dynamics induced by ischemia-reperfusion.

引用

页码：H1215 / H1231

页数：17

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