期刊
BASIC RESEARCH IN CARDIOLOGY
卷 104, 期 2, 页码 169-180出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00395-009-0011-9
关键词
Autophagy; Mitochondria; Homeostasis; Lysosomes; Preconditioning; Cardioprotection
资金
- NIH [P01HL85577, R01HL060590, R01AG033283, R21AG030187, R01HL034579]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL060590, P01HL085577, R01HL034579] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R21AG030187, R01AG033283] Funding Source: NIH RePORTER
Autophagy is a critical cellular housekeeping process that is essential for removal of damaged or unwanted organelles and protein aggregates. Under conditions of starvation, it is also a mechanism to break down proteins to generate amino acids for synthesis of new and more urgently needed proteins. In the heart, autophagy is upregulated by starvation, reactive oxygen species, hypoxia, exercise, and ischemic preconditioning, the latter a well-known potent cardioprotective phenomenon. The observation that upregulation of autophagy confers protection against ischemia/reperfusion injury and inhibition of autophagy is associated with a loss of cardioprotection conferred by pharmacological conditioning suggests that the pathway plays a key role in enhancing the heart's tolerance to ischemia. While many of the antecedent signaling pathways of preconditioning are well-defined, the mechanisms by which preconditioning and autophagy converge to protect the heart are unknown. In this review we discuss mechanisms that potentially underlie the linkage between cardioprotection and autophagy in the heart.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据