Role of macrophages in aortic dissection pathogenesis:insights from preclinical studies to translational prospective

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外文摘要：Aortic dissection is a critical vascular disease that is characterized by a high mortality rate and inflammation significantly influences its onset and progression.Recent studies highlight the integral role of macrophages,key players in the immune system,in the pathological landscape of aortic dissection.These cells are involved in crucial processes,such as the remodeling of the extracellular matrix,immunocyte infiltration,and phenotypic switching of smooth muscle cells,which are essential for the structural integrity and functional dynamics of the aortic wall.Despite these insights,the specific contributions of macrophages to the development and progression of aortic dissection remains unclear.This review explores the pathogenesis of aortic dissection with a focus on macrophages and describes their origins,phenotypic variations,and potential roles based on the most recent research findings.Furthermore,we discuss key molecules related to macrophages during aortic dissection,their interactions with other cellular components within the aorta,and the implications of these interactions for future therapeutic strategies.This comprehensive analysis aimed to improve our understanding of macrophages in aortic dissection and promote the development of targeted interventions.

外文关键词：

aortic dissectionmacrophagesextracellular matrixcytokines

作者：

Shiyi Li、Weiguo Fu、Lixin Wang

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作者单位：

Department of Vascular Surgery,Zhongshan Hospital,Fudan University,Shanghai 200032,China

Vascular Surgery Institute of Fudan University,Shanghai 200032,China

National Clinical Research Center for Interventional Medicine,Shanghai 200032,China

Key Laboratory of Panvascular Disease Precision Medicine,Zhongshan Hospital Xiamen,Fudan University,Xiamen 361015,China

Fudan Zhangjiang Institute,Shanghai 201203,China

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出版年：

2024

DOI：

10.1007/s11427-024-2693-5

中国科学:生命科学(英文版)

中国科学院

中国科学:生命科学(英文版)

CSTPCD

影响因子：0.806

ISSN：1674-7305

年,卷(期)：2024.67(11)