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在与代谢功能障碍相关的脂肪性肝病中,MRPL44通过BNIP3介导的线粒细胞衰变来调节脂质代谢

Siqi Liu¹, Lianggui Xiao², Qiuchen Cheng¹

¹Institute of Digestive Disease, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.

Frontiers in nutrition

|October 20, 2025

概括

线性与代谢功能障碍相关的脂肪性肝病作斗争. 这项研究揭示了MRPL44蛋白通过增强甲状腺食来减轻肝脏脂肪的积累,提供了一个新的治疗点.

科学领域:

肝病学和代谢疾病研究.
线粒体生物学和细胞应激反应.

背景情况:

与代谢功能障碍相关的脂肪性肝病 (MASLD) 与受损的线粒细胞吸收有关.
线粒体核糖体蛋白44 (MRPL44) 在脂质代谢中的作用以前是未知的.

研究的目的:

研究MRPL44在MASLD进展中的作用.
探索MRPL44在脂质新陈代谢和线粒细胞衰变中的调节功能.

主要方法:

使用带有油脂/棕酸诱导的HepG2细胞模型.
采用高脂肪饮食小鼠模型,具有透视病毒介导的MRPL44过度表达.
进行了线粒的测定,以评估MRPL44的影响.

主要成果:

在HepG2细胞中,MRPL44过度表达减少了甘油三积累,并增强了脂肪酸氧化.
肝脏特异性MRPL44过度表达在小鼠减弱高脂肪饮食诱导的肝脂沉积.
MRPL44激活了依赖BNIP3的线粒细胞衰变途径,促进了线粒体生物发生,减少了脂质积累.

结论:

确定MRPL44是脂质新陈代谢的新型调节剂.
在MRPL44中,通过线粒细胞吸收 (mitophagy) 证明了它对MASLD的保护作用.
MRPL44代表了对MASLD的潜在治疗点.

关键词:

在 MRPL44 课程中学习.脂肪酸氧化过程中的脂肪酸氧化.与代谢功能障碍相关的脂肪性肝病.线粒体质量的质量线粒细胞衰变 (mitophagy) 是一种神经衰变的过程.

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