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氧化应激在主动脉夹层中的作用:一个潜在的治疗靶点。

The role of oxidative stress in aortic dissection: a potential therapeutic target.

作者信息

Xu Shengnan, Han Xueyu, Wang Xiukun, Yu Yi, Qu Chuan, Liu Xin, Yang Bo

机构信息

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.

Cardiovascular Research Institute, Wuhan University, Wuhan, China.

出版信息

Front Cardiovasc Med. 2024 Jul 12;11:1410477. doi: 10.3389/fcvm.2024.1410477. eCollection 2024.

DOI:10.3389/fcvm.2024.1410477
PMID:39070552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11272543/
Abstract

The incidence of aortic dissection (AD) is steadily increasing, driven by the rising prevalence of chronic conditions such as hypertension and the global aging of the population. Oxidative stress emerges as a pivotal pathophysiological mechanism contributing to the progression of AD. Oxidative stress triggers apoptosis in vascular smooth muscle cells, reshapes the extracellular matrix (ECM), and governs ECM degradation and remodeling, subsequently impacting aortic compliance. Furthermore, oxidative stress not only facilitates the infiltration of macrophages and mononuclear lymphocytes but also disrupts the integral structure and functionality of endothelial cells, thereby inducing endothelial cell dysfunction and furthering the degeneration of the middle layer of the aortic wall. Investigating antioxidants holds promise as a therapeutic avenue for addressing AD.

摘要

主动脉夹层(AD)的发病率正在稳步上升,这是由高血压等慢性疾病的患病率上升以及全球人口老龄化所驱动的。氧化应激已成为导致AD进展的关键病理生理机制。氧化应激触发血管平滑肌细胞凋亡,重塑细胞外基质(ECM),并控制ECM的降解和重塑,随后影响主动脉顺应性。此外,氧化应激不仅促进巨噬细胞和单核淋巴细胞的浸润,还破坏内皮细胞的整体结构和功能,从而诱导内皮细胞功能障碍并加剧主动脉壁中层的退化。研究抗氧化剂有望成为治疗AD的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/ecbf1988e3cf/fcvm-11-1410477-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/923c44e1838e/fcvm-11-1410477-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/f30798679e08/fcvm-11-1410477-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/74ac3309a2ea/fcvm-11-1410477-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/ecbf1988e3cf/fcvm-11-1410477-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/923c44e1838e/fcvm-11-1410477-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/f30798679e08/fcvm-11-1410477-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/74ac3309a2ea/fcvm-11-1410477-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9835/11272543/ecbf1988e3cf/fcvm-11-1410477-g004.jpg

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