4.6 Article

Autophagy - A novel protective mechanism in chronic ischemia

期刊

CELL CYCLE
卷 5, 期 11, 页码 1175-1177

出版社

TAYLOR & FRANCIS INC
DOI: 10.4161/cc.5.11.2787

关键词

autophagy; apoptosis; chronic myocardial ischemia; cardioprotection

资金

  1. NHLBI NIH HHS [HL33107, HL59139, HL65182, HL69020, HL65183] Funding Source: Medline
  2. NIA NIH HHS [AG14121, AG023137] Funding Source: Medline
  3. NICHD NIH HHS [HD01457] Funding Source: Medline

向作者/读者索取更多资源

During the search for cardioprotective mechanisms in a porcine model of chronic myocardial ischemia and hibernating myocardium, we discovered evidence for autophagy, which could be involved in the protection against apoptosis. Autophagy is a cellular degradation process responsible for the turnover of unnecessary or dysfunctional organelles and cytoplasmic proteins, which become sequestered in a double-membrane-bound vesicle, termed autophagosome, and subsequently degrade upon fusion with lysosomes. The dauer phase in C. elegans shares similarities with the induction of autophagy in chronically ischemic (hibernating) myocardium. In this sense, autophagy is an essential mechanism for survival which is activated by environmental stresses and confers stress resistance to the organism. Our study provided insight into understanding of the protective mechanism of autophagy in chronic ischemia.

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