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Macrophage NRF1 promotes mitochondrial protein turnover via the ubiquitin proteasome system to limit mitochondrial stress and inflammation

文献类型：期刊论文

作者Yan, Jiawei6; Zhang, Xin6; Wang, Huiying6; Jia, Xinglong5; Wang, Ruohong3,4; Wu, Shuangyang2; Zhu, Zheng-Jiang1; Tan, Minjia5; Horng, Tiffany6
刊名CELL REPORTS
出版日期2024-10-22
卷号43期号:10页码:23
ISSN号2211-1247
DOI10.1016/j.celrep.2024.114780
通讯作者Horng, Tiffany(tsyhorng@shanghaitech.edu.cn)
英文摘要Macrophage elaboration of inflammatory responses is dynamically regulated, shifting from acute induction to delayed suppression during the course of infection. Here, we show that such regulation of inflammation is modulated by dynamic shifts in metabolism. In macrophages exposed to the bacterial product lipopolysaccharide (LPS), an initial induction of protein biosynthesis is followed by compensatory induction of the transcription factor nuclear factor erythroid 2-like 1 (NRF1), leading to increased flux through the ubiquitin proteasome system (UPS). A major target of NRF1-mediated UPS flux is the mitochondrial proteome, and in the absence of NRF1, ubiquitinated mitochondrial proteins accumulate to trigger severe mitochondrial stress. Such mitochondrial stress engages the integrated stress response-ATF4 axis, which limits mitochondrial translation to attenuate mitochondrial stress but amplifies inflammatory responses to augment susceptibility to septic shock. Therefore, NRF1 mediates a dynamic regulation of mitochondrial proteostasis in inflammatory macrophages that contributes to curbing inflammatory responses.
WOS关键词SUCCINATE-DEHYDROGENASE ; TRANSCRIPTION FACTOR ; CELL ; METABOLISM ; ACTIVATION ; EXPRESSION ; MORPHOLOGY
资助项目NSFC[32225026] ; NSFC[92057105] ; NSFC[32070895] ; NSFC[32300750] ; MOST[2021YFA0804700] ; Foreign Experts Programs by Science & Technologic Commission of Shanghai Municipality (STCSM)[22WZ2504000] ; Shanghai Frontiers Science Center for Biomacromolecules and Precision Medicine at ShanghaiTech University ; Shanghai Clinical Research and Trial Center, Shanghai, People's Republic of China ; European Union Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant[847548] ; Shanghai Municipal Science and Technology Major Project[2019SHZDZX02] ; Shanghai Key Laboratory of Aging Studies[19DZ2260400]
WOS研究方向Cell Biology
语种英语
WOS记录号WOS:001325116600001
出版者CELL PRESS
源URL[http://119.78.100.183/handle/2S10ELR8/313654]  
专题新药研究国家重点实验室
通讯作者Horng, Tiffany
作者单位1.Shanghai Key Lab Aging Studies, Shanghai 201210, Peoples R China
2.Austrian Acad Sci, Gregor Mendel Inst Mol Plant Biol, Dr Bohr Gasse 3, AT-1030 Vienna, Austria
3.Chinese Acad Sci, Interdisciplinary Res Ctr Biol & Chem, Shanghai Inst Organ Chem, Shanghai 200032, Peoples R China
4.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
5.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China
6.ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai 201210, Peoples R China
推荐引用方式
GB/T 7714		 Yan, Jiawei,Zhang, Xin,Wang, Huiying,et al. Macrophage NRF1 promotes mitochondrial protein turnover via the ubiquitin proteasome system to limit mitochondrial stress and inflammation[J]. CELL REPORTS,2024,43(10):23.
APA Yan, Jiawei.,Zhang, Xin.,Wang, Huiying.,Jia, Xinglong.,Wang, Ruohong.,...&Horng, Tiffany.(2024).Macrophage NRF1 promotes mitochondrial protein turnover via the ubiquitin proteasome system to limit mitochondrial stress and inflammation.CELL REPORTS,43(10),23.
MLA Yan, Jiawei,et al."Macrophage NRF1 promotes mitochondrial protein turnover via the ubiquitin proteasome system to limit mitochondrial stress and inflammation".CELL REPORTS 43.10(2024):23.

入库方式： OAI收割

来源：上海药物研究所

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