Department of Pharmacology and Therapeutics, The Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada.
Antioxid Redox Signal. 2011 Jun;14(11):2245-50. doi: 10.1089/ars.2010.3479. Epub 2011 Jan 7.
Autophagy is a highly orchestrated cellular process by which proteins and organelles are degraded via an elaborate lysosomal pathway to generate free amino acids and sugars for ATP during metabolic stress. At present, the exact role of autophagy in the heart is highly debated but suggested to play a key role in regulating cell turnover in cardiomyopathies and heart failure. The signaling pathways and molecular effectors that govern autophagy are incomplete, as are the mechanisms that determine whether autophagy promotes or prevents cell death. The mitochondrion has been identified as a key organelle centrally involved in regulating autophagy. Certain members of the Bcl-2 gene family, including Beclin-1, Bcl-2 nineteen kilodaltons interacting protein (Bnip3), and Nix/Bnip3L, provoke mitochondrial perturbations leading to permeability transition pore opening, resulting in apoptosis, autophagy, or both. These and other aspects of autophagy processes have been discussed.
自噬是一种高度协调的细胞过程，通过这个过程，蛋白质和细胞器通过精细的溶酶体途径降解，在代谢应激期间生成游离氨基酸和糖以产生 ATP。目前，自噬在心脏中的确切作用仍存在争议，但被认为在心肌病和心力衰竭中调节细胞更新方面发挥关键作用。调控自噬的信号通路和分子效应物并不完整，决定自噬是促进还是防止细胞死亡的机制也不完整。线粒体已被确定为中央参与调节自噬的关键细胞器。Bcl-2 基因家族的某些成员，包括 Beclin-1、Bcl-2 十九千道尔顿相互作用蛋白（Bnip3）和 Nix/Bnip3L，引发导致通透性转换孔打开的线粒体扰动，导致细胞凋亡、自噬或两者兼有。这些和自噬过程的其他方面已经被讨论过了。
