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Myofibroblasts restore connective tissue integrity and contract the wound during tissue repair. Excessive myofibroblast activity is characteristic of the majority of fibrocontractive diseases. Following tissue injury, local fibroblasts and other mesenchymal cells, blood-circulating cells, epithelial and endothelial cells acquire smooth muscle features. Hallmark of this transition is the neo-expression of α-smooth muscle actin, generating high contractile activity in stress fibres. Of clinical relevance are the retractile phenomena caused by excessive myofibroblast activity characterizing the vast majority of fibrocontractive diseases. This includes fibrosis affecting vital organs, such as heart, liver, kidney and lung.

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Other fibrotic phenomena reduce life quality in scleroderma, hypertrophic scars (remarkably severe after large burn wounds), chronic asthma and Dupuytren's disease. Moreover, myofibroblasts at the tumor invasion front are activated by the transformed epithelium to stimulate tumor growth and invasion by promoting angiogenesis and tumor cell migration. In tissue engineering and regenerative medicine considerable effort is required to prevent myofibroblast formation, either arising from mesenchymal stem cells that are implanted to repair tissues or at the interface between the implant and the host connective tissue. But don't be fooled - the myofibroblast is not necessarily the 'bad guy' as it contributes to physiological wound healing and its absence has been associated with development of chronic wounds. In all these conditons, controlling the tissue activity of myofibroblasts will be beneficial for the outcome of the body repair process.