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RNF128通过调节PPARα功能来调节适应性代谢对禁食的反应

Yu-Lung Lin^1,2, Pei-Yao Liu^3,4, Yu-Ling Tsai^5,6

¹The Ph.D. Program for Translational Medicine, College for Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.

Cell death and differentiation

|September 10, 2025

概括

研究人员发现,RING手指蛋白128 (RNF128) 在禁食期间降解转录因子PPARα. 这种RNF128介导的降解对于肝脏的代谢适应和脂质调节至关重要.

科学领域:

代谢调节代谢调节代谢调节
分子生物学分子生物学
脂质代谢脂质代谢是一种

背景情况:

过氧体增殖器激活受体α (PPARα) 调节关键的代谢过程,如脂肪酸氧化和生成在禁食期间.
控制PPARα活性的精确分子机制,特别是在营养缺乏期间的调节,尚未完全理解.

研究的目的:

在禁食期间识别PPARα功能的新型调节剂.
阐明RING指蛋白128 (RNF128) 在PPARα介导的代谢适应中的作用.

主要方法:

*体外研究:研究了RNF128和PPARα之间的相互作用,评估了PPARα的多比基因化和降解.
*基因表达分析:测量了RNF128对PPARα向基因的影响,包括纤维细胞生长因子21 (FGF21) 和与脂质代谢相关的基因.
*体内研究:利用RNF128缺乏的小鼠和腺相关病毒 (AAV) 血清型8介导的过度表达模型来评估禁食期间的代谢参数.

主要成果:

*确定了RNF128作为一种新型PPARα结合蛋白,它促进PPARα聚基化和随后的降解.
* RNF128过度表达抑制了PPARα活性,在禁食期间抑制了FGF21表达和脂质代谢基因.
*抑制RNF128增强了PPARα依赖的脂肪酸氧化和饥饿细胞中的生成.
*在体内,RNF128缺乏改善了脂质概况,并在禁食期间促进了脂肪酸氧化和生成.
*小鼠中AAV8介导的RNF128过度表达导致脂质水平升高,代谢基因表达减少.

结论:

在禁食期间,RNF128作为PPARα的关键负调节剂,通过促进其降解而起作用.
通过调节PPARα活性,RNF128在肝脏对营养缺乏的代谢适应中发挥着至关重要的作用.
RNF128代表了与禁食反应受损相关的代谢障碍的潜在治疗标.

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