The suppression of hyperlipid diet‐induced ferroptosis of vascular smooth muscle cells protests against atherosclerosis independent of p53/SCL7A11/GPX4 axis

Jia You; Siyu Ouyang; Zhongcheng XieChenxi ZhiJiang YuXiaoqian TanPin LiXiaoyan LinWentao MaZhiyang LiuQin HouNan XieTianhong PengXi ChenLiang LiWei Xie

首页> 外文期刊>Journal of cellular physiology. >The suppression of hyperlipid diet‐induced ferroptosis of vascular smooth muscle cells protests against atherosclerosis independent of p53/SCL7A11/GPX4 axis

【24h】

The suppression of hyperlipid diet‐induced ferroptosis of vascular smooth muscle cells protests against atherosclerosis independent of p53/SCL7A11/GPX4 axis

机译：The suppression of hyperlipid diet‐induced ferroptosis of vascular smooth muscle cells protests against atherosclerosis independent of p53/SCL7A11/GPX4 axis

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相关主题

摘要

Abstract Ferroptosis as a novel programmed cell death that involves metabolic dysfunction due to iron‐dependent excessive lipid peroxidation has been implicated in atherosclerosis (AS) development characterized by disrupted lipid metabolism, but the atherogenic role of ferroptosis in vascular smooth muscle cells (VSMCs), which are principal components of atherosclerotic plaque fibrous cap, remains unclear. The aim of this study was to determine the effects of ferroptosis on AS induced by lipid overload, and the effects of that on VSMCs ferroptosis. We found intraperitoneal injection of Fer‐1, a ferroptosis inhibitor, ameliorated obviously high‐fat diet‐induced high plasma levels of triglycerides, total cholesterol, low‐density lipoprotein, glucose and atherosclerotic lesions in ApoE?/? mice. Moreover, in vivo and in vitro, Fer‐1 reduced the iron accumulation of atherosclerotic lesions through affecting the expression of TFR1, FTH, and FTL in VSMCs. Interestingly, Fer‐1 did augment nuclear factor E2‐related factor 2/ferroptosis suppressor protein 1 to enhance endogenous resistance to lipid peroxidation, but not classic p53/SCL7A11/GPX4. Those observations indicated inhibition of VSMCs ferroptosis can improve AS lesions independent of p53/SLC7A11/GPX4, which preliminarily revealed the potential mechanism of ferroptosis in aortic VSMCs on AS and provided new therapeutic strategies and targets for AS.

著录项

来源
《Journal of cellular physiology.》 |2023年第8期|1891-1908|共18页
作者
Jia You; Siyu Ouyang; Zhongcheng XieChenxi ZhiJiang YuXiaoqian TanPin LiXiaoyan LinWentao MaZhiyang LiuQin HouNan XieTianhong PengXi ChenLiang LiWei Xie;
展开▼
作者单位

Clinical Anatomy & Reproductive Medicine Application Institute, Hengyang Medical School,University;

Department of Physiology, Hengyang Medical School,University of South China;

展开▼
收录信息
原文格式 PDF
正文语种英语
中图分类细胞生物学;
关键词
atherosclerosis; ferroptosis; p53/SLC7A11/GPX4;

The suppression of hyperlipid diet‐induced ferroptosis of vascular smooth muscle cells protests against atherosclerosis independent of p53/SCL7A11/GPX4 axis

摘要

著录项

相关主题

期刊订阅