Autophagy: Definition, Molecular Machinery, and Potential Role in Myocardial Ischemia-Reperfusion Injury

被引:93
作者
Dong, Yi [1 ,2 ]
Undyala, Vishnu V. [1 ]
Gottlieb, Roberta A. [3 ]
Mentzer, Robert M., Jr. [1 ,3 ,4 ]
Przyklenk, Karin [1 ,2 ,5 ]
机构
[1] Wayne State Univ, Sch Med, Cardiovasc Res Inst, Detroit, MI 48201 USA
[2] Wayne State Univ, Sch Med, Dept Physiol, Detroit, MI 48201 USA
[3] San Diego State Univ, BioSci Ctr, San Diego, CA 92182 USA
[4] Wayne State Univ, Sch Med, Dept Surg, Detroit, MI 48201 USA
[5] Wayne State Univ, Sch Med, Dept Emergency Med, Detroit, MI 48201 USA
关键词
autophagy; myocardial ischemia; myocardial reperfusion; apoptosis; signal transduction; PERMEABILITY TRANSITION PORE; UNFOLDED PROTEIN RESPONSE; CELL-DEATH; ISCHEMIA/REPERFUSION INJURY; MOUSE HEART; LYSOSOMAL ALTERATIONS; REOXYGENATED HEARTS; SIGNALING PATHWAYS; CARDIAC MYOCYTES; HYDROGEN-SULFIDE;
D O I
10.1177/1074248410370327
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Autophagy is the endogenous, tightly regulated cellular "housekeeping" process responsible for the degradation of damaged and dysfunctional cellular organelles and protein aggregates. There is a growing consensus that autophagy is upregulated in the setting of myocardial ischemia-reperfusion. Moreover, emerging data suggest that autophagy may serve as an adaptive process and confer increased resistance to ischemia-reperfusion injury. Our aims in this review are to (1) provide a brief synopsis of process of autophagy (including an overview of the key molecular mediators of this catabolic process and its relationship with other cardiac signaling pathways) and (2) most importantly, summarize the current evidence for versus against the intriguing concept of autophagy-mediated cardioprotection.
引用
收藏
页码:220 / 230
页数:11
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