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通过重塑肝脂组成以抑制铁亡,FATP5 缺乏缓解了MASH

Yiran Liu¹, Mingyu Zhang¹, Chen Zhu¹

¹Department of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei Province, China; Institute of Liver and Gastrointestinal Diseases, Hubei Key Laboratory of Hepato-Pancreato-Biliary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei Province, China.

Free radical biology & medicine

|August 21, 2025

概括

脂肪酸运输蛋白5 (FATP5) 通过增加铁死促进了与代谢功能失调相关的脂肪肝炎 (MASH). 抑制FATP5或增强甲酸脱酶1 (SCD1) 可以缓解MASH,表明FATP5是治疗点.

科学领域:

肝病学
脂肪新陈代谢
细胞死亡途径

背景情况:

代谢功能障碍相关的脂肪肝炎 (MASH) 是一种严重的脂肪肝疾病.
脂肪酸运输蛋白5 (FATP5) 在MASH上调,但其在疾病进展中的作用尚不清楚.
肝脂失调有助于MASH的发生.

研究的目的:

研究FATP5在MASH进展中的功能作用.
探索MASH中FATP5,脂质代谢和铁的关系.
确定MASH的潜在治疗点.

主要方法:

在体外 (HepG2细胞) 和体内 (小鼠模型) 使用MASH模型.
使用铁酶抑制剂 (ferrostatin-1) 和基因操纵 (FATP5缺乏,SCD1过度表达).
进行非向性脂组学和基因表达分析 (SREBP1,SCD1).

主要成果:

在MASH模型中证实了FATP5的上调.
FATP5 缺乏和铁的抑制减弱了MASH.
降低FATP5,激活SREBP1/SCD1轴并抑制铁.
通过抑制铁死,SCD1的过度表达改善了MASH.

结论:

通过促进铁亡,FATP5在MASH的发病过程中起着至关重要的作用.
针对FATP5或调节SREBP1/SCD1途径为MASH提供了潜在的治疗策略.
FATP5被确定为MASH的一个有前途的治疗点.

关键词:

在FATP 铁症脂肪代谢美国一个 SCD1

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