生物
ABCA1
肝X受体
基因敲除
脂质代谢
巨噬细胞
胆固醇
载脂蛋白E
细胞生物学
内分泌学
内科学
生物化学
核受体
基因
细胞凋亡
医学
体外
转录因子
运输机
疾病
作者
Shuyun Lin,Lianjie Hou,Yu Wang,Huiling Lin,Jiefeng Deng,Shuang� Li,Haijiao Long,Guojun Zhao
出处
期刊:Gene
[Elsevier]
日期:2024-02-23
卷期号:909: 148302-148302
标识
DOI:10.1016/j.gene.2024.148302
摘要
Changes in circulating let-7c were significantly associated with the alter in lipid profile, but its role in intracellular lipid metabolism remains unknown. This work was conducted to explore the effects of let-7c on the lipid accumulation in macrophages and uncover the underlying mechanism. Our results showed that let-7c inhibition relieved atherosclerosis progression in apoE-/- mice. In ox-LDL-treatment macrophages, let-7c knockdown suppressed lipid accumulation but does no affect cholesterol intake. Consistent with this, overexpression of let-7c promoted lipid accumulation by reducing the expression of LXRα and ABCA1/G1. Mechanistically, let-7c targeted PGC-1α to repress the expression of LXRα and ABCA1/G1, thereby regulating cholesterol homeostasis in macrophages. Taken together, these findings suggest that antagonism of let-7c reduces atherosclerosis and macrophage lipid accumulation through the PGC-1α/LXRα/ABCA1/G1 axis.
科研通智能强力驱动
Strongly Powered by AbleSci AI