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After severe skin injury such as burns, our body rapidly but imperfectly repairs the damage, leaving behind a stiff scar. Scarring is a clinical burden because skin is losing vital functions. If scars form in internal organs, e.g., in the heart after myocardial infarct, the outcome can be lethal. During normal tissue repair, local fibroblasts and other precursor cells are activated into so-called myofibroblasts to secrete large amounts of collagen that is organized into fibrous structures by the strong pulling forces developed by mature myofibroblasts. Both actions are beneficial since they prevent our tissues from breaking but can lead to scarring when the repair demands of our body exceed its regenerative potential. To control scar formation, it will be important to uncouple the beneficial production of collagen that is needed to fill injured tissue space from the contraction of the matrix that disfigures the skin. First evidence from our lab indicates that the mechanical state of the scar (stiffness) controls whether myofibroblasts produce collagen or contract.
Boris Hinz
Reutlingen University
Life Sciences
Education
University of Toronto
Globalink Research Award
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