Abstract
The discovery of the myofibroblast has allowed definition of the cell responsible for wound contraction and for the development of fibrotic changes. This review summarizes the main features of the myofibroblast and the mechanisms of myofibroblast generation. Myofibroblasts originate from a variety of cells according to the organ and the type of lesion. The mechanisms of myofibroblast contraction, which appear clearly different to those of smooth muscle cell contraction, are described. Finally, we summarize the possible strategies in order to reduce myofibroblast activities and thus influence several pathologies, such as hypertrophic scars and organ fibrosis.
Highlights
Wound healing has interested the medical praxis since the beginning of human history, but for many centuries the effort of physicians has concentrated more on empirical therapeutic strategies rather than on the understanding of its biological mechanisms
The formation and evolution of granulation tissue has been described in the second half of the 18th century, mainly thanks to the British surgeon John Hunter, and in the last century it has been shown that wound contraction is due to an active contraction of granulation tissue, mainly thanks to the work of the French surgeon Alexis Carrel[1]
The discovery of the myofibroblast more than forty years ago allowed the identification of the cell responsible for this phenomenon[2]
Summary
Wound healing has interested the medical praxis since the beginning of human history, but for many centuries the effort of physicians has concentrated more on empirical therapeutic strategies rather than on the understanding of its biological mechanisms. The recent observation that tropomyosin 1.6/7 isoforms play an essential role in the stable incorporation of α-SM actin into fibroblast stress fibers[70] points to a new target for the reduction of α-SM actin expression in myofibroblasts with the consequent reduction of their remodeling activity[71]. Another way to regulate myofibroblast remodeling activity could be the control of the Rho/ROCK/myosin light chain phosphatase pathway. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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