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December 1996

Signaling Networks in Barrier Homeostasis: The Mystery Widens

Author Affiliations

Department of Veterans Affairs Medical Center Dermatology Service 190 4150 Clement St San Francisco, CA 94121

Arch Dermatol. 1996;132(12):1505-1506. doi:10.1001/archderm.1996.03890360097017

IN THIS ISSUE of the Archives, Suetake et al1 provide detailed results about barrier function in various types of healing wounds. While these data per se are of considerable interest, the authors also report that an abnormal permeability barrier persists over hypertrophic scars and keloids, long after reepithelialization of wounds is complete. Whereas their results do not address the potential mechanisms for the persistent functional defect, 3 possible explanations, which need not be mutually exclusive, should be considered: (1) a primary defect in the dermis of patients with hypertrophic scars and keloids leads to signals that negatively influence barrier homeostasis; (2) the excess collagen and glycosaminoglycans found in the dermis of keloids impede the ability of key nutritional ingredients, metabolic precursors, and/or growth factors to reach the epidermis; and (3) a defect in the epidermis leads to a persistent barrier abnormality, resulting in a sustained release of signaling molecules

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