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      The myofibroblast: Paradigm for a mechanically active cell

      Journal of Biomechanics
      Elsevier BV

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          Abstract

          Tissues lose mechanical integrity when our body is injured. To rapidly restore mechanical stability a multitude of cell types can jump into action by acquiring a reparative phenotype-the myofibroblast. Here, I review the known biomechanics of myofibroblast differentiation and action and speculate on underlying mechanisms. Hallmarks of the myofibroblast are secretion of extracellular matrix, development of adhesion structures with the substrate, and formation of contractile bundles composed of actin and myosin. These cytoskeletal features not only enable the myofibroblast to remodel and contract the extracellular matrix but to adapt its activity to changes in the mechanical microenvironment. Rapid repair comes at the cost of tissue contracture due to the inability of the myofibroblast to regenerate tissue. If contracture and ECM remodeling become progressive and manifests as organ fibrosis, the outcome of myofibroblast activity will have more severe consequences than the initial damage. Whereas the pathological consequences of myofibroblast occurrence are of great interest for physicians, their mechano-responsive features render them attractive for physicists and bioengineers. Their well developed cytoskeleton and responsiveness to a plethora of cytokines fascinate cell biologists and biochemists. Finally, the question of the myofibroblast origin intrigues stem cell biologists and developmental biologists-what else can you ask from a truly interdisciplinary cell? Copyright 2009 Elsevier Ltd. All rights reserved.

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          Author and article information

          Journal
          Journal of Biomechanics
          Journal of Biomechanics
          Elsevier BV
          00219290
          January 2010
          January 2010
          : 43
          : 1
          : 146-155
          Article
          10.1016/j.jbiomech.2009.09.020
          19800625
          34fca5c3-a3f2-40c1-b432-57252ab6c50a
          © 2010

          https://www.elsevier.com/tdm/userlicense/1.0/

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