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Cardiovascular Research 1998 38(3):545-548; doi:10.1016/S0008-6363(98)00065-0
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Evolution and clinical implications of the myofibroblast concept

Giulio Gabbiani*

Department of Pathology, University of Geneva-CMU, 1 rue Michel-Servet, 1211 Geneva 4, Switzerland

* Corresponding author. Tel.: +41 (22) 702–5742; Fax: +41 (22) 702–5746; E-mail: giulio.gabbiani@medecine.unige.ch

Received 31 December 1997; accepted 16 February 1998

The first 150 words of the full text of this article appear below.


    1 Development of the myofibroblast concept
 
The phenomena of wound contraction and scar retraction are known since old ages (for review see [1]). In the first part of our century, the work of Carrel and Lecomte du Noüy has contributed to the notion that the forces producing wound contraction are generated within the granulation tissue itself [2]. These forces were generally considered to depend on extracellular matrix rearrangements; however, Abercrombie and co-workers reported, in the fifties, that fibroblasts exert tractional forces in vitro [3]. Similarly, Hoffmann-Beerling showed that addition of ATP to permeabilized fibroblasts in culture produces a contraction of their cytoplasm [4]. In this context, and in the context of emerging work on cytoskeleton morphology and function [5], the ultrastructural observation made in our laboratory in 1971 that during granulation tissue evolution fibroblasts acquire smooth muscle (SM) cell features, such as the presence of cytoplasmic microfilament bundles [6], lead . . . [Full Text of this Article]


    2 Agents influencing myofibroblast evolution
 

    3 Mechanisms of myofibroblast activity
 

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