Autophagy - A novel protective mechanism in chronic ischemia

被引:44
作者
Yan, Lin
Sadoshima, Junichi
Vatner, Dorothy E.
Vatner, Stephen F.
机构
[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA
[2] Univ Med & Dent New Jersey, New Jersey Med Sch, Cardiovasc Res Inst, Newark, NJ 07103 USA
关键词
autophagy; apoptosis; chronic myocardial ischemia; cardioprotection;
D O I
10.4161/cc.5.11.2787
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:1175 / 1177
页数:3
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