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[Perspective] Fibroblasts become fat to reduce scarring

ScienceNOW - Fetched: February 16th, 2017, 5:00pm UTC

Following cutaneous injury in adult mammals, one of two outcomes can occur: successful healing with scar formation or nonsuccessful healing and a chronic wound. In humans, scar formation can be classified in terms of “normal scar” formation versus pathologically increased fibrosis, as seen in hypertrophic scarring and keloids (1). Although scarring does not look or function like surrounding unwounded skin, it allows one to survive injury (and hence, procreate). However, extensive scarring from burns and conditions such as scleroderma or epidermolysis bulosa are not only unsightly but also contribute to substantial morbidity owing to loss of functionality in affected tissues and limbs. In the United States alone, there are greater than 50 million incisions and lacerations each year, all of which heal with some degree of scarring (2). Thus, scarring represents an enormous and growing medical burden in our aging population. On page 748 of this issue, Plikus et al. (3) demonstrate that scarring could be mitigated by controlling fibroblast plasticity. This has very exciting translational implications for treating scar formation during wound repair. Authors: Charles K. F. Chan, Michael T. Longaker

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