IFI27 Integrates Succinate and Fatty Acid Oxidation to Promote Adipocyte Thermogenic Adaption.
IFI27 Integrates Succinate and Fatty Acid Oxidation to Promote Adipocyte Thermogenic Adaption.
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IFI27 整合琥珀酸和脂肪酸氧化，促进脂肪细胞生热适应。
DOI：
10.1002/advs.202301855
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发表时间：
2023-10
期刊：
影响因子：
15.1
通讯作者：
Pan, Dongning
中科院分区：
文献类型：
--
作者：
Cui, Xuan;Liu, Haojie;Shi, Ting;Zhao, Qingwen;Li, Feiyan;Lv, Wenjing;Yu, Chao;Huang, Haiyan;Tang, Qi-Qun;Pan, Dongning
Mitochondria are the pivot organelles to control metabolism and energy homeostasis. The capacity of mitochondrial metabolic adaptions to cold stress is essential for adipocyte thermogenesis. How brown adipocytes keep mitochondrial fitness upon a challenge of cold‐induced oxidative stress has not been well characterized. This manuscript shows that IFI27 plays an important role in cristae morphogenesis, keeping intact succinate dehydrogenase (SDH) function and active fatty acid oxidation to sustain thermogenesis in brown adipocytes. IFI27 protein interaction map identifies SDHB and HADHA as its binding partners. IFI27 physically links SDHB to chaperone TNF receptor associated protein 1 (TRAP1), which shields SDHB from oxidative damage‐triggered degradation. Moreover, IFI27 increases hydroxyacyl‐CoA dehydrogenase trifunctional multienzyme complex subunit alpha (HADHA) catalytic activity in β‐oxidation pathway. The reduced SDH level and fatty acid oxidation in Ifi27‐knockout brown fat results in impaired oxygen consumption and defective thermogenesis. Thus, IFI27 is a novel regulator of mitochondrial metabolism and thermogenesis. Mitochondria are central organelles in energy metabolism which determine the capacity of adipocyte thermogenesis. Mitochondrial matrix protein IFI27 protects SDHB from oxidative damage, and promotes fatty acid oxidation (FAO) by increasing HADHA activity. Loss of IFI27 in adipocytes elicits compromises succinate and fatty acid oxidation in mitochondria and decreases adaptability to cold challenge.
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影响因子：
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作者：
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通讯作者：
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影响因子：
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通讯作者：
Puigserver P
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64.8
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通讯作者：
Spiegelman BM