期刊
AUTOPHAGY
卷 4, 期 4, 页码 416-421出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.5655
关键词
autophagy; ischemia; reperfusion; heart; cardiac myocytcs; mitochondria; cell death; beclin 1
类别
资金
- NHLBI NIH HHS [HL060590, R01 HL087023, R01 HL071091, R01 HL060590, P01 HL085577, R01 HL061518, HL087023, HL085577, HL071091] Funding Source: Medline
- NIA NIH HHS [AG025168, R01 AG033283, R01 AG021568] Funding Source: Medline
Autophagy is an important process in the heart which is responsible for the normal turnover of long lived proteins and organelles. Inhibition of autophagy leads to the accumulation of protein aggregates and dysfunctional organelles which can cause cell death. Autophagy occurs at low basal levels under normal conditions in the heart, but is rapidly upregulated in response to stress such as nutrient deprivation, hypoxia and pressure overload. Autophagy is a prominent feature of myocardial ischemia and reperfusion. Although enhanced autophagy is often seen in dying cardiac myocytes, the functional significance of autophagy under these conditions is not dear. Upregulation of autophagy has been reported to protect cardiac cells against death as well as be the cause of it. Here, we review the evidence that autophagy can have both beneficial and detrimental roles in the myocardium, and discuss potential mechanisms by which autophagy provides protection in cells.
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