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Chchd10:一种新的代谢传感器调节脂肪组织恒温

Xiaoping Wu^1,2, Zixuan Zhang^1,2, Jingjing Li³

¹State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong SAR, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|February 22, 2025

概括

卷曲-卷曲-螺旋-卷曲-卷曲-螺旋域含有10 (Chchd10) 缺乏症有助于脂肪组织 (AT) 的重塑,并对抗肥胖. 在AT中失去Chchd10可以通过增强能量储存和减少细胞损伤来防止代谢障碍.

科学领域:

代谢研究的研究.
脂肪组织生物学脂肪组织生物学
肥胖研究的研究.

背景情况:

脂肪组织 (AT) 稳态对于代谢健康至关重要,而其在肥胖中失调导致代谢压力.
肥胖与代谢障碍有关,强调需要了解AT重塑机制.

研究的目的:

为了确定脂肪组织在过多的能量摄入过程中重塑的新型调节者.
研究含有10 (Chchd10) 的Coiled-coil-helix-coiled-coil-helix域在饮食诱导的肥胖和代谢功能障碍中的作用.

主要方法:

使用的小鼠模型养高脂肪饮食 (HFD) 来研究脂肪组织变化.
分析基因表达,脂肪生成和蛋白质碳化作为对Chchd10缺乏的反应.
研究了分子通路,包括TDP43/Raptor/p62/Keap1/NRF2轴,参与Chchd10介导的AT重塑.

主要成果:

在HFD条件下,chchd10水平在白色脂肪组织 (WAT) 中降低.
缺少CHCHD10加速皮下AT的脂肪生成,并在内脏AT上调节谷氨S转移酶A4 (GSTA4),减轻肥胖和代谢障碍.
缺少Chchd10会激活TDP43/Raptor/p62/Keap1/NRF2轴,从而增强脂肪生成和GSTA4的表达.
缺少Chchd10的有益影响在过度化的脂肪细胞中被废除,p62水平降低.

结论:

Chchd10充当一种新陈代谢传感器,维持脂肪组织的平衡.
脂肪组织中Chchd10的损失促进了适应性重塑,以预防肥胖和相关的代谢障碍.
由于肥胖患者的p62损失导致Chchd10介导的AT重塑受损,突显了代谢功能障碍中的关键机制.

关键词:

第10章孩子们这是GSTA4的GSTA4.这就是NRF2的NRF2.在TDP43中使用.脂质生成 (adipogenesis) 是一种脂肪组织重塑的重塑肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖在P62上,P62就是P62 蛋白质碳基化蛋白质的碳基化

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