Parkin regulates adiposity by coordinating mitophagy with mitochondrial biogenesis in white adipocytes.
Parkin regulates adiposity by coordinating mitophagy with mitochondrial biogenesis in white adipocytes.
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帕金通过协调白色脂肪细胞的线粒体自噬和线粒体生物合成来调节肥胖。
DOI：
10.1038/s41467-022-34468-2
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发表时间：
2022-11-04
影响因子：
16.6
通讯作者：
Zhou, Zhenqi
中科院分区：
文献类型：
--
作者：
Moore, Timothy M.;Cheng, Lijing;Wolf, Dane M.;Ngo, Jennifer;Segawa, Mayuko;Zhu, Xiaopeng;Strumwasser, Alexander R.;Cao, Yang;Clifford, Bethan L.;Ma, Alice;Scumpia, Philip;Shirihai, Orian S.;Vallim, Thomas Q. de Aguiar;Laakso, Markku;Lusis, Aldons J.;Hevener, Andrea L.;Zhou, Zhenqi
Parkin, an E3 ubiquitin ligase, plays an essential role in mitochondrial quality control. However, the mechanisms by which Parkin connects mitochondrial homeostasis with cellular metabolism in adipose tissue remain unclear. Here, we demonstrate that Park2 gene (encodes Parkin) deletion specifically from adipose tissue protects mice against high-fat diet and aging-induced obesity. Despite a mild reduction in mitophagy, mitochondrial DNA content and mitochondrial function are increased in Park2 deficient white adipocytes. Moreover, Park2 gene deletion elevates mitochondrial biogenesis by increasing Pgc1α protein stability through mitochondrial superoxide-activated NAD(P)H quinone dehydrogenase 1 (Nqo1). Both in vitro and in vivo studies show that Nqo1 overexpression elevates Pgc1α protein level and mitochondrial DNA content and enhances mitochondrial activity in mouse and human adipocytes. Taken together, our findings indicate that Parkin regulates mitochondrial homeostasis by balancing mitophagy and Pgc1α-mediated mitochondrial biogenesis in white adipocytes, suggesting a potential therapeutic target in adipocytes to combat obesity and obesity-associated disorders. Parkin plays a role in mitophagy and has been shown to control adipose tissue browning and thermogenesis. Here the authors report that Parkin coordinates mitophagy with Pgc1α-mediated mitochondrial biogenesis in white adipocytes to regulate adiposity.
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影响因子：
7.7
作者：
Hwang JH;Kim DW;Jo EJ;Kim YK;Jo YS;Park JH;Yoo SK;Park MK;Kwak TH;Kho YL;Han J;Choi HS;Lee SH;Kim JM;Lee I;Kyung T;Jang C;Chung J;Kweon GR;Shong M
通讯作者：
Shong M
DOI：
10.1161/atvbaha.116.308749
发表时间：
2017-03
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Den Hartigh LJ;Omer M;Goodspeed L;Wang S;Wietecha T;O'Brien KD;Han CY
通讯作者：
Han CY
影响因子：
7.3
作者：
Altshuler-Keylin S;Kajimura S
通讯作者：
Kajimura S
Mitophagy 受体 FUNDC1 受 PGC-1α/NRF1 调节，以微调线粒体稳态。
影响因子：
7.7
作者：
Liu, Lei;Li, Yanjun;Chen, Quan
通讯作者：
Chen, Quan
影响因子：
4.8
作者：
Corsa, Callie A. S.;Pearson, Gemma L.;Soleimanpour, Scott A.
通讯作者：
Soleimanpour, Scott A.