Scientific article
Meta-analysis
OA Policy
English

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

Published in

Arteriosclerosis, thrombosis, and vascular biology, vol. 31, no. 11, p. 2391-2396

Publication date

2011

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.

Keywords

  • Animals
  • Cardiovascular Diseases/pathology/physiopathology
  • Cell Communication/physiology
  • Cell Differentiation/physiology
  • Connective Tissue/pathology/physiopathology
  • Fibroblasts/pathology/physiology
  • Humans
  • Myofibroblasts/pathology/physiology
  • Tunica Intima/pathology/physiopathology
  • Tunica Media/pathology/physiopathology

Citation (ISO format)

COEN, Matteo, GABBIANI, Giulio, BOCHATON-PIALLAT, Marie-Luce. Myofibroblast-mediated adventitial remodeling: an underestimated player in arterial pathology. In: Arteriosclerosis, thrombosis, and vascular biology, 2011, vol. 31, n° 11, p. 2391–2396. doi: 10.1161/ATVBAHA.111.231548

Main files (1)

Article (Published version)

Identifiers

Journal ISSN

1079-5642
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596downloads

Technical informations

Creation

06/11/2012 17:43:00

First validation

06/11/2012 17:43:00

Update

14/03/2023 19:57:20

Status update

14/03/2023 19:57:20

Last indexation

29/01/2025 17:09:14
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