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阿斯素-FABP5相互作用通过PPARα调节线粒体脂肪酸氧化,有助于MASLD的发展

Yuan-Yuan Yu¹, Min Feng¹, Yi Chen¹

¹Department of Pharmacology, SKLFZCD, (State Key Laboratory -Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, 150081, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|April 15, 2025

概括

禁食诱导的激素阿斯素在代谢功能障碍相关的脂肪性肝病 (MASLD) 中升高,并损害肝脏脂肪酸氧化. 针对阿斯素或FABP5提供了潜在的MASLD疗法.

科学领域:

肝病学肝病学是一种肝病学.
代谢疾病代谢疾病
分子生物学分子生物学

背景情况:

与代谢功能障碍相关的脂肪性肝病 (MASLD) 涉及复杂的肝脏代谢变化.
禁食释放的激素阿斯素向肝脏,但其在MASLD中的作用尚不清楚.

研究的目的:

调查阿斯素在MASLD病变发生过程中的作用.
探索阿斯素作为MASLD的潜在生物标志物和治疗点.

主要方法:

在MASLD患者和动物模型中测量了血阿斯素水平.
在小鼠中利用肝细胞特异性阿斯素过度表达和淘汰模型.
研究了涉及FABP5,PPARα和脂肪酸氧化 (FAO) 的分子机制.
评估了针对FABP5.5的GalNAc-siRNA的治疗潜力.

主要成果:

在MASLD中,血阿斯素水平和肝脏阿斯素表达升高.
肝细胞阿斯素过度表达会损害肝脏的FAO;敲击会增强FAO并改善MASLD治疗结果.
阿斯素与FABP5相互作用,导致异常的核定位和抑制PPARα转录活性,破坏肝脏FAO.
用GalNAc-siRNAs准肝脏FABP5可以改善肝脏肥胖症.

结论:

升高的阿斯素因破坏肝脏FAO而涉及MASLD的致病性.
阿斯素作为MASLD诊断和预后的潜在生物标志物.
抑制肝脏阿斯素或FABP5为MASLD提供了有前途的治疗策略.

关键词:

在FABP5中,FABP5是FABP5中的一个.这是一种PPARα.作为一个prosin.芬诺纤维酸盐的使用方法肝脏肥胖症肝脏肥胖症胰岛素耐药性是一种胰岛素耐药性.线粒体脂肪酸β-氧化作用

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