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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.