Rady Faculty of Health Sciences, Department of Physiology and Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, Man., Canada; Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, Man., Canada.
Rady Faculty of Health Sciences, Department of Physiology and Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, Man., Canada; Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, Man., Canada.
Trends Cardiovasc Med. 2018 May;28(4):246-260. doi: 10.1016/j.tcm.2017.11.008. Epub 2017 Dec 6.
Autophagy is a catabolic process for eliminating macromolecules and damaged organelles by a highly regulated lysosomal pathway. Importantly, autophagy serves as an integral quality control mechanism by recycling cellular constituents for energy consumption and cellular rejuvenation under basal and stress conditions. Nevertheless, there is growing evidence that under certain conditions autophagy can switch from an adaptive survival mechanism to maladaptive process that promotes cell death. Furthermore, defects in autophagy have been linked to mitochondria injury and cell death associated with aging. In this review, we describe the role of autophagy as a physiological mechanism for maintaining homeostasis with its specific involvement in mitochondrial quality control and cardiac aging.
自噬是一种通过高度调控的溶酶体途径消除大分子和受损细胞器的分解代谢过程。重要的是,自噬作为一种整体质量控制机制,通过在基础和应激条件下回收细胞成分来消耗能量和使细胞恢复活力。然而,越来越多的证据表明,在某些情况下,自噬可以从适应性生存机制转变为促进细胞死亡的失调过程。此外,自噬缺陷与衰老相关的线粒体损伤和细胞死亡有关。在这篇综述中,我们描述了自噬作为维持体内平衡的生理机制的作用,以及它在维持线粒体质量控制和心脏衰老中的特定作用。