期刊
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
卷 60, 期 2, 页码 110-117出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FJC.0b013e31824cc427
关键词
cardiac myocytes; autophagy; heart failure; Bnip3; heart; programmed cell death; hypoxia; mitochondria
资金
- Canadian Institutes of Health Research (CIHR)
- Heart and Stroke Foundation of Canada (HSFC)
- CIHR-MHRC Fellowship
- IMPACT Strategic Training Program
Autophagy constitutes a catabolic process involving lysosomal degradation of damaged and redundant cytosolic components into biomolecules, via an elaborate lysosomal pathway. Autophagy is a highly regulated and evolutionary conserved process crucial for normal tissue homeostasis and cell life. Certain members of the Bcl-2 gene family, including the BH3 only protein Bnip3 regulate autophagy during cardiac stress during ischemic or hypoxic injury as means of discarding damaged mitochondria and organelles to avert cell death. Defects in the regulation of autophagy have been associated with a number of human pathologies including cancer, neurodegenerative diseases, and heart failure. Here, we discuss the molecular regulation of autophagy in the heart and cellular demise from too much a good thing.
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