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内质网应激在动脉粥样硬化发病机制中的研究进展

Recent progress of endoplasmic reticulum stress in the mechanism of atherosclerosis.

作者信息

Ni Lin, Yang Luqun, Lin Yuanyuan

机构信息

Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, China.

出版信息

Front Cardiovasc Med. 2024 Jul 12;11:1413441. doi: 10.3389/fcvm.2024.1413441. eCollection 2024.

DOI:10.3389/fcvm.2024.1413441
PMID:39070554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11282489/
Abstract

The research progress of endoplasmic reticulum (ER) stress in atherosclerosis (AS) is of great concern. The ER, a critical cellular organelle, plays a role in important biological processes including protein synthesis, folding, and modification. Various pathological factors may cause ER stress, and sustained or excessive ER stress triggers the unfolded protein response, ultimately resulting in apoptosis and disease. Recently, researchers have discovered the importance of ER stress in the onset and advancement of AS. ER stress contributes to the occurrence of AS through different pathways such as apoptosis, inflammatory response, oxidative stress, and autophagy. Therefore, this review focuses on the mechanisms of ER stress in the development of AS and related therapeutic targets, which will contribute to a deeper understanding of the disease's pathogenesis and provide novel strategies for preventing and treating AS.

摘要

内质网(ER)应激在动脉粥样硬化(AS)中的研究进展备受关注。内质网作为一种关键的细胞器,在包括蛋白质合成、折叠和修饰等重要生物学过程中发挥作用。多种病理因素可导致内质网应激,持续或过度的内质网应激会触发未折叠蛋白反应,最终导致细胞凋亡和疾病。近年来,研究人员发现内质网应激在动脉粥样硬化的发生和发展过程中具有重要作用。内质网应激通过凋亡、炎症反应、氧化应激和自噬等不同途径促进动脉粥样硬化的发生。因此,本综述聚焦于内质网应激在动脉粥样硬化发展过程中的机制及相关治疗靶点,这将有助于更深入地理解该疾病的发病机制,并为预防和治疗动脉粥样硬化提供新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/11282489/0f01f9566507/fcvm-11-1413441-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/11282489/94811b1d0b97/fcvm-11-1413441-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/11282489/d6fff46afcdf/fcvm-11-1413441-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/11282489/0f01f9566507/fcvm-11-1413441-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/11282489/94811b1d0b97/fcvm-11-1413441-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/11282489/d6fff46afcdf/fcvm-11-1413441-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/363d/11282489/0f01f9566507/fcvm-11-1413441-g003.jpg

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