Departments of Physiology and Pharmacology and Therapeutics, Institute of Cardiovascular Sciences, St Boniface General Hospital Research Center, Room 3016, 351 Taché Avenue, Winnipeg, Manitoba, Canada R2H 2A6.
J Cardiovasc Pharmacol. 2012 Aug;60(2):110-7. doi: 10.1097/FJC.0b013e31824cc427.
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."
自噬是一个溶酶体降解途径，涉及将受损和冗余的细胞质成分降解为生物分子，是一个具有高度调控和进化保守的细胞过程，对于正常的组织稳态和细胞生存至关重要。Bcl-2 基因家族的某些成员，包括 BH3 仅蛋白 Bnip3，在缺血或缺氧损伤等心脏应激期间调节自噬，以去除受损的线粒体和细胞器，避免细胞死亡。自噬调节的缺陷与包括癌症、神经退行性疾病和心力衰竭在内的许多人类疾病有关。在这里，我们讨论了心脏中的自噬分子调控以及“物极必反”导致的细胞死亡。
