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作 者:Wen Li Mingyue Dong Kaiyu Gao Jialiang Guan Ying Liu
机构地区:[1]State Key Laboratory of Membrane Biology,New Cornerstone Science Laboratory,Institute of Molecular Medicine,College of Future Technology,Peking University,Beijing 100871,China [2]Peking-Tsinghua Center for Life Sciences,Academy for Advanced Interdisciplinary Studies,Peking University,Beijing 100871,China [3]Beijing Advanced Innovation Center for Genomics,Beijing 100871,China [4]PKU-Tsinghua-NIBS Graduate Program,Academy for Advanced Interdisciplinary Studies,Peking University,Beijing 100871,China
出 处:《Life Metabolism》2024年第4期55-61,共7页生命代谢(英文)
基 金:supported by the National Natural Science Foundation of China(32293212,92254305,and 31925012);the HHMI International Research Scholar Program(55008739)to Y.L.Y.L.was also supported by the Peking-Tsinghua Center for Life Sciences,Beijing Advanced Innovation Center for Genomics,and the Tencent Foundation through the XPLORER PRIZE.
摘 要:Dear Editor,Organisms have evolved mitochondrial stress response pathways to surveil mitochondrial function and activate repair programs upon detection of mitochondrial dysfunction[1].Failure to respond to mitochondrial perturbation has been implicated in aging and age-related diseases[2,3].Mitochondrial perturbation in mammals primarily activates the integrated stress response(ISR).
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