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肌成纤维细胞介导的血管外膜重构:动脉病理学中被低估的角色。

Myofibroblast-mediated adventitial remodeling: an underestimated player in arterial pathology.

机构信息

Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.

出版信息

Arterioscler Thromb Vasc Biol. 2011 Nov;31(11):2391-6. doi: 10.1161/ATVBAHA.111.231548.

DOI:10.1161/ATVBAHA.111.231548
PMID:21868702
Abstract

The arterial adventitia has been long considered an essentially supportive tissue; however, more and more data suggest that it plays a major role in the modulation of the vascular tone by complex interactions with structures located within intima and media. The purpose of this review is to summarize these data and to describe the mechanisms involved in adventitia/media and adventitia/intima cross-talk. In response to a plethora of stimuli, the adventitia undergoes remodeling processes, resulting in positive (adaptive) remodeling, negative (constrictive) remodeling, or both. The differentiation of the adventitial fibroblast into myofibroblast (MF), a key player of wound healing and fibrosis development, is a hallmark of negative remodeling; this can lead to vessel stenosis and thus contribute to major cardiovascular diseases. The mechanisms of fibroblast-to-MF differentiation and the role of the MF in adventitial remodeling are highlighted herein.

摘要

动脉外膜长期以来一直被认为是一种基本的支持组织;然而,越来越多的数据表明,它通过与内膜和中膜内的结构的复杂相互作用,在调节血管张力方面起着重要作用。本文综述了这些数据,并描述了外膜/中膜和外膜/内膜相互作用中涉及的机制。动脉外膜对大量刺激发生重塑过程,导致积极(适应性)重塑、消极(收缩性)重塑或两者兼有。外膜成纤维细胞分化为肌成纤维细胞(MF)是消极重塑的一个标志,MF 是伤口愈合和纤维化发展的关键参与者;这可导致血管狭窄,从而促成主要心血管疾病。本文重点介绍了成纤维细胞向 MF 分化的机制以及 MF 在动脉外膜重塑中的作用。

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