期刊
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY AND THERAPEUTICS
卷 15, 期 3, 页码 220-230出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1074248410370327
关键词
autophagy; myocardial ischemia; myocardial reperfusion; apoptosis; signal transduction
资金
- NHLBI NIH HHS [R01 HL060590] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL060590] Funding Source: NIH RePORTER
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.
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