Autophagy plays a crucial role in maintaining cellular homeostasis in response to various stimuli. Compared to research on nutrient deprivation-induced autophagy, the understanding of the molecular mechanisms and physiological/pathological significance of autophagy triggered by energy deprivation remains limited. A primary focus of our lab is to elucidate how cells sense energy deprivation and initiate autophagy. Using the model organisms Saccharomyces cerevisiae and mammalian cells, we found that cellular reactive oxygen species (ROS), DNA damage sensor Mec1, and mitochondrial aerobic respiration play essential roles in the autophagy induced by energy deprivation. This review aims to provide a concise overview of these research findings.
作为细胞内重要的物质降解途径，自噬在维持细胞稳态过程中起着至关重要的作用。然而，相较于物质匮乏诱导的自噬，我们对能量匮乏诱导自噬的分子机制和生理病理意义的认识非常有限。因此，我们实验室主要探究细胞如何感知能量匮乏并启动自噬发生。通过酿酒酵母和哺乳动物细胞两种模式生物，我们发现在能量匮乏诱导的自噬发生中，细胞的活性氧（ROS）、DNA损伤感受器Mec1和线粒体有氧呼吸是必需的。本文旨在对这些研究成果进行简要总结，并提出该研究领域今后的重点发展方向。.
Keywords: Autophagy; Chaperonin-containing TCP-1, subunit 2 (CCT2); Glucose starvation; Solid aggrephagy.