Aortic dissection and vascular smooth muscle cell apoptosis: in-depth exploration of their relationship and potential therapeutic strategies.
10.3760/cma.j.cn121430-20241015-00842
- Author:
Haodong ZHOU
1
;
Zanxin WANG
2
Author Information
1. Faculty of Medicine, Shenzhen University, Shenzhen 518053, Guangdong, China.
2. Hong Kong University Shenzhen Hospital Cardiovascular Medicine Center, Shenzhen 518053, Guangdong, China. Corresponding author: Wang Zanxin, Email: wangzx@hku-szh.org.
- Publication Type:English Abstract
- MeSH:
Apoptosis;
Humans;
Muscle, Smooth, Vascular/pathology*;
Aortic Dissection/therapy*;
Oxidative Stress;
Myocytes, Smooth Muscle/pathology*;
Aortic Aneurysm/pathology*
- From:
Chinese Critical Care Medicine
2025;37(3):225-231
- CountryChina
- Language:Chinese
-
Abstract:
Aortic dissection (AD) is a life-threatening cardiovascular disease characterized a tear in the aortic intima, which leads to the formation of two separate channels within the aortic wall due to blood flow. The mortality rate of AD is high, especially when dissection ruptures, as it can rapidly trigger acute cardiac and vascular complications, ultimately leading to death. Therefore, understanding the pathogenesis of AD and identifying potential therapeutic strategies is of critical clinical importance. Vascular smooth muscle cell (VSMC) play a central role in the structural and functional integrity of the aortic wall, and dysfunction of VSMC is closely associated with the development of AD. Recent studies suggest that the functional alterations of VSMC involve multiple mechanisms, including apoptosis, oxidative stress, and aberrant intracellular signaling, all of which play key roles in the disruption of the aortic wall structure. This review focuses on the role of VSMC in AD, particularly the specific involvement of VSMC apoptosis in the progression of AD, and further explores therapeutic strategies targeting the pathological processes of VSMC in AD, such as the inhibition of inflammatory mediators and oxidative stress. Despite some progress in current treatments, effectively intervening in the pathological progression of VSMC remains a significant challenge. Future research will further investigate these mechanisms, providing new insights and strategies for the treatment of AD. Studying the role of VSMC in AD is crucial for the development of novel therapeutic approaches.
