粒体自噬
线粒体分裂
线粒体生物发生
甲状腺激素受体
PPARGC1A型
细胞生物学
自噬
受体
辅活化剂
线粒体
柠檬酸循环
氧化磷酸化
生物
生物化学
转录因子
新陈代谢
基因
细胞凋亡
作者
Brijesh Kumar Singh,Rohit A. Sinha,Madhulika Tripathi,Arturo Mendoza,Kenji Ohba,Jann A. C. Sy,Sherwin Xie,Jin Zhou,Jia Pei Ho,Ching‐yi Chang,Yajun Wu,Vincent Giguère,Boon‐Huat Bay,Jean-Marc Vanacker,Sujoy Ghosh,Karine Gauthier,Anthony N. Hollenberg,Donald P. McDonnell,Paul M. Yen
出处
期刊:Science Signaling
[American Association for the Advancement of Science]
日期:2018-06-26
卷期号:11 (536)
被引量:149
标识
DOI:10.1126/scisignal.aam5855
摘要
inhibited TH-induced autophagic clearance of mitochondria through mitophagy and decreased OXPHOS. These findings show that many of the mitochondrial actions of TH are mediated through stimulation of ESRRA expression and activity, and co-regulation of mitochondrial turnover through the PPARGC1A-ESRRA-ULK1 pathway is mediated by their regulation of mitochondrial fission and mitophagy. Hormonal or pharmacologic induction of ESRRA expression or activity could improve mitochondrial quality in metabolic disorders.
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