自噬在心力衰竭中的微观、宏观作用研究

Microcosmic and Macroscopic Effects of Autophagy in Heart Failure

自噬是在溶酶体的介导下降解细胞内受损的分子物质和细胞内容物,进而维持细胞内环境的稳态。随着自噬作用机制的逐步揭示,其在心力衰竭中的分子作用机制也备受关注。心肌细胞在缺血、缺氧、饥饿等应激状态下,相应的细胞器,如线粒体、内质网、泛素-蛋白酶体遭受破坏,细胞内环境在发生改变过程中可观察到自噬活动的增加,并清除受损的蛋白质和细胞器等,进而阻止心力衰竭的进展。自噬不仅可以维持心肌细胞的内环境,而且也参与了心肌细胞的重构和凋亡,对维持心肌细胞的形态和功能发挥重要作用。因此,如何调控心力衰竭中心肌细胞的自噬活动,将可能成为未来心力衰竭治疗的突破点。

Autophagy is a degradation of damaged molecule substance and cellular content under the mediate of lyso- some, and thus maintains the homeostasis of the intracellular environment. As the mechanism of autophagy is being gradually revealed, the molecular mechanism of autophagy in heart failure receives more and more attention. Myocardial cell organ- eUes, such as mitochondria,endoplasmie reticulum and ubiquitin-proteosome, are damaged under stress states of ischemia, anoxia and starvation. The autophagy-related activities increase with the changing in cell internal environment, and by elimi- nating impaired proteins and organelles, the progress of cardiac failure is prevented. Autophagy not only maintains the inter- nal environment of myocardial cells, but also participates in the reconstruction and apoptosis of myocardial cells, which is important for remaining sthe hape and function of the cells. Therefore, how to regulate the myocardial cell autophagy in heart failure will probably be the breakthrough point for heart failure treatment in the future.