Jin Chenglong, Zhu Min, Ye Jinling, Song Zhiwen, Zheng Chuntian, Chen Wei
State Key Laboratory of Swine and Poultry Breeding Industry, Guangzhou 510640, China.
Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China.
Curr Issues Mol Biol. 2024 Aug 13;46(8):8780-8793. doi: 10.3390/cimb46080519.
Autophagy is a kind of "self-eating" phenomenon that is ubiquitous in eukaryotic cells. It mainly manifests in the damaged proteins or organelles in the cell being wrapped and transported by the autophagosome to the lysosome for degradation. Many factors cause autophagy in cells, and the mechanism of nutrient-deficiency-induced autophagy has been a research focus. It has been reported that amino-acid-deficiency-induced cellular autophagy is mainly mediated through the mammalian rapamycin target protein complex 1 (mTORC1) signaling pathway. In addition, some researchers also found that non-mTORC1 signaling pathways also regulate autophagy, and the mechanism of autophagy occurrence induced by the deficiency of different amino acids is not precisely the same. Therefore, this review aims to summarize the process of various amino acids regulating cell autophagy and provide a narrative review on the molecular mechanism of amino acids regulating autophagy.
自噬是一种在真核细胞中普遍存在的“自噬”现象。它主要表现为细胞内受损的蛋白质或细胞器被自噬体包裹并运输到溶酶体进行降解。许多因素可引起细胞自噬，其中营养缺乏诱导自噬的机制一直是研究热点。据报道，氨基酸缺乏诱导的细胞自噬主要通过哺乳动物雷帕霉素靶蛋白复合物1（mTORC1）信号通路介导。此外，一些研究人员还发现非mTORC1信号通路也参与调节自噬，且不同氨基酸缺乏诱导自噬发生的机制并不完全相同。因此，本综述旨在总结各种氨基酸调节细胞自噬的过程，并对氨基酸调节自噬的分子机制进行叙述性综述。
