Suppr超能文献

EndMT:HS 针对动脉粥样硬化的潜在靶点。

EndMT: Potential Target of HS against Atherosclerosis.

机构信息

Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, Hengyang Medical College, University of South China, Hengyang City, Hunan Province 421001, China.

Department of Cardiology, Affiliated Nanhua Hospital, University of South China, Hengyang City, Hunan Province 421001, China.

出版信息

Curr Med Chem. 2021;28(18):3666-3680. doi: 10.2174/0929867327999201116194634.

Abstract

Atherosclerosis is a chronic arterial wall illness that forms atherosclerotic plaques within the arteries. Plaque formation and endothelial dysfunction are atherosclerosis' characteristics. It is believed that the occurrence and development of atherosclerosis mainly include endothelial cell damage, lipoprotein deposition, inflammation and fibrous cap formation, but its molecular mechanism has not been elucidated. Therefore, protecting the vascular endothelium from damage is one of the key factors against atherosclerosis. The factors and processes involved in vascular endothelial injury are complex. Finding out the key factors and mechanisms of atherosclerosis caused by vascular endothelial injury is an important target for reversing and preventing atherosclerosis. Changes in cell adhesion are the early characteristics of EndMT, and cell adhesion is related to vascular endothelial injury and atherosclerosis. Recent researches have exhibited that endothelial-mesenchymal transition (EndMT) can urge atherosclerosis' progress, and it is expected that inhibition of EndMT will be an object for anti-atherosclerosis. We speculate whether inhibition of EndMT can become an effective target for reversing atherosclerosis by improving cell adhesion changes and vascular endothelial injury. Studies have shown that HS has a strong cardiovascular protective effect. As HS has anti- inflammatory, anti-oxidant, inhibiting foam cell formation, regulating ion channels and enhancing cell adhesion and endothelial functions, the current research on HS in cardiovascular aspects is increasing, but anti-atherosclerosis's molecular mechanism and the function of H2S in EndMT have not been explicit. In order to explore the mechanism of HS against atherosclerosis, to find an effective target to reverse atherosclerosis, we sum up the progress of EndMT promoting atherosclerosis, and Hydrogen sulfide's potential anti- EndMT effect is discussed in this review.

摘要

动脉粥样硬化是一种慢性动脉壁疾病,它在动脉内形成动脉粥样硬化斑块。斑块形成和内皮功能障碍是动脉粥样硬化的特征。据信,动脉粥样硬化的发生和发展主要包括内皮细胞损伤、脂蛋白沉积、炎症和纤维帽形成,但它的分子机制尚未阐明。因此,保护血管内皮免受损伤是防治动脉粥样硬化的关键因素之一。血管内皮损伤涉及的因素和过程复杂。找出血管内皮损伤引起的动脉粥样硬化的关键因素和机制是逆转和预防动脉粥样硬化的重要目标。细胞黏附的变化是 EndMT 的早期特征,细胞黏附与血管内皮损伤和动脉粥样硬化有关。最近的研究表明,内皮-间充质转化(EndMT)可以促使动脉粥样硬化的进展,抑制 EndMT 有望成为抗动脉粥样硬化的靶点。我们推测,通过改善细胞黏附变化和血管内皮损伤,抑制 EndMT 是否可以成为逆转动脉粥样硬化的有效靶点。研究表明,HS 具有很强的心血管保护作用。由于 HS 具有抗炎、抗氧化、抑制泡沫细胞形成、调节离子通道以及增强细胞黏附和内皮功能的作用,目前对心血管方面 HS 的研究正在增加,但 HS 抗动脉粥样硬化的分子机制和 H2S 在 EndMT 中的作用尚不清楚。为了探讨 HS 防治动脉粥样硬化的机制,寻找逆转动脉粥样硬化的有效靶点,我们总结了 EndMT 促进动脉粥样硬化的进展,并在这篇综述中讨论了 H2S 的潜在抗 EndMT 作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验