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微RNA-18a-5p调节肝脏脂质积累,以应对高脂肪饮食

Giuseppe Petito¹, Nunzia Magnacca¹, Arianna Cuomo¹

¹Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "Luigi Vanvitelli", Caserta, Italy.

Frontiers in physiology

|September 22, 2025

概括

微RNA-18a-5p (miR-18a-5p) 在代谢功能障碍相关的脂肪性肝病 (MASLD) 中被下调,导致脂质积累和ER压力. 恢复miR-18a-5p水平可以改善这些MASLD病理.

科学领域:

肝病学肝病学是一种肝病学.
分子生物学分子生物学
生物化学生物化学

背景情况:

代谢功能障碍相关的脂肪性肝病 (MASLD),以前称为NAFLD,涉及肝脏脂肪积累和ER压力.
在MASLD病原体的关键参与者包括SREBP1c和PERK/eIF2α通路.
不调节的脂质代谢和ER压力是MASLD进展的核心.

研究的目的:

研究微RNA-18a-5p (miR-18a-5p) 在MASLD中的作用.
确定miR-18a-5p对MASLD模型中的脂质积累和ER压力的影响.

主要方法:

在使用高脂肪饮食 (HFD) 的雄性Wistar大鼠中诱导MASLD.
在使用脂肪酸处理的HepG2细胞建立了体外MASLD模型.
分析了miR-18a-5p表达及其下游影响.

主要成果:

在HFD诱导的MASLD大鼠和脂肪酸治疗的HepG2细胞中,miR-18a-5p的下调.
降低调节与增加的SREBP1c,PERK通路激活,脂质积累,亡和自功能受损相关.
在两种模型中,miR-18a-5p的过度表达逆转了这些有害影响.

结论:

在MASLD中,miR-18a-5p是脂质稳定和ER压力的关键调节者.
miR-18a-5p代表了MASLD的潜在治疗标.
了解这些分子机制对于开发MASLD治疗至关重要.

关键词:

压力ERER压力ERER压力灭症 (apoptosis) 是一种死亡的过程.自自是自的过程.脂肪脂肪是一种脂肪.肝脏肝脏肝脏肝脏肝脏肝脏这是一个小RNARNA.甘油三胺的使用方法

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