期刊
AGEING RESEARCH REVIEWS
卷 81, 期 -, 页码 -出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2022.101702
关键词
Mitochondrial unfolded protein response; Mitochondria stress; Neurodegenerative diseases; Aging; ATFS-1
资金
- One Hundred Person Project of Hebei Province [E2016100019]
Mitochondria are involved in various cellular functions and are regulated by the mitochondrial unfolded protein response (UPRmt) in response to environmental stresses. The regulatory mechanisms and factors involved in UPRmt differ between Caenorhabditis elegans and mammals. Exploring UPRmt can provide new directions and strategies for the treatment of human diseases.
Mitochondria, which serve as the energy factories of cells, are involved in cell differentiation, calcium homeostasis, amino acid and fatty acid metabolism and apoptosis. In response to environmental stresses, mitochondrial homeostasis is regulated at both the organelle and molecular levels to effectively maintain the number and function of mitochondria. The mitochondrial unfolded protein response (UPRmt) is an adaptive intracellular stress mechanism that responds to stress signals by promoting the transcription of genes encoding mitochondrial chaperones and proteases. The mechanism of the UPRmt in Caenorhabditis elegans (C. elegans) has been clarified over time, and the main regulatory factors include ATFS-1, UBL-5 and DVE-1. In mammals, the activation of the UPRmt involves eIF2a phosphorylation and the uORF-regulated expression of CHOP, ATF4 and ATF5. Several additional factors, such as SIRT3 and HSF1, are also involved in regulating the UPRmt. A deep and comprehensive exploration of the UPRmt can provide new directions and strategies for the treatment of human diseases, including aging, neurodegenerative diseases, cardiovascular diseases and diabetes. In this review, we mainly discuss the function of UPRmt, describe the regulatory mechanisms of UPRmt in C. elegans and mammals, and summarize the relationship between UPRmt and various human diseases.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据