Autophagy in ischemic heart disease.
Autophagy in ischemic heart disease.
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DOI：
10.1161/circresaha.108.187427
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发表时间：
2009-01-30
影响因子：
20.1
通讯作者：
Gottlieb RA
中科院分区：
文献类型：
--
作者：
Gustafsson AB;Gottlieb RA
自噬是哺乳动物细胞降解和回收大分子和细胞器的主要分解代谢途径。它在清除蛋白质聚集体以及受损或过量的细胞器以维持细胞内稳态和保持细胞健康方面起着关键作用。在心脏中，自噬在正常情况下以低水平发生，该过程中的缺陷导致心功能障碍和心力衰竭。然而，该途径在环境应激条件下快速上调，包括ATP耗竭、活性氧和线粒体渗透性转换孔开放。虽然自噬在各种病理生理条件下增强，例如在缺血和再灌注期间，但自噬增加的功能作用尚不清楚，目前正在进行深入研究。在这篇综述中，我们讨论了缺血和再灌注心脏自噬的证据，确定调节自噬的因素，并分析自噬可能在心脏细胞中发挥的潜在作用。
Autophagy is a major catabolic pathway by which mammalian cells degrade and recycle macromolecules and organelles. It plays a critical role in removing protein aggregates as well as damaged or excess organelles in order to maintain intracellular homeostasis and to keep the cell healthy. In the heart, autophagy occurs at low levels under normal conditions, and defects in this process cause cardiac dysfunction and heart failure. However, this pathway is rapidly upregulated under environmental stress conditions, including ATP depletion, reactive oxygen species, and mitochondrial permeability transition pore opening. Although autophagy is enhanced in various pathophysiological conditions such as during ischemia and reperfusion, the functional role of increased autophagy is not clear and is currently under intense investigation. In this review, we discuss the evidence for autophagy in the heart in response to ischemia and reperfusion, identify factors that regulate autophagy, and analyze the potential roles autophagy might play in cardiac cells.