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Wound-Associated Skin Fibrosis: Mechanisms and Treatments Based on Modulating the Inflammatory Response

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Skin fibrosis, in its mildest form, may present only a minor aesthetic problem, but in the most severe cases it can lead to debilitating pathologies of the skin, for example keloid and hypertrophic scars, and systemic sclerosis. In recent years, extensive basic research aimed at understanding the molecular mechanisms underlying fibrosis has revealed an impressive but baffling number of genes, molecules, and cell types that may contribute to this problem. However, one recurring and consistent theme in these studies is that inflammatory cells and their secreted mediators appear to be leading culprits in activating dermal fibroblasts to become fibrotic. This review will first describe the histology of normal versus fibrotic skin, and will also describe the process of wound repair, a primary cause of skin fibrosis. We will then focus on what is currently known about the molecular mechanisms underlying skin fibrosis, with particular attention paid to how inflammation contributes. Finally, current treatment strategies and emerging therapeutic targets will be discussed.

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Keywords: Arachidonic acid; D-penicillamine; Fos-related antigen-2; Intracellular adhesion molecule-1; Skin; Surgical resection; activator protein 1; and photo therapies; antisense oligodeoxynucleotide; azathioprine; colchicine; collagen; collagen type I; cyclooxygenase; cyclosporine; cytokine; early growth response gene-1; epidermal growth factor; fibronectin; fibrosis; inflammation; keloid scars; leukotrienes; lipoxygenase; matrix-degrading metalloproteinases; peroxisome proliferator-activated receptor gamma; prostaglandins; radiation therapy; scar; spider veins; telangiectasia; thromboxane; urokinase-type plasminogen activator receptor; wound

Document Type: Research Article

Publication date: December 1, 2010

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  • This journal is devoted to timely reviews of experimental and clinical studies in the field of endocrine, metabolic, and immune disorders. Specific emphasis is placed on humoral and cellular targets for natural, synthetic, and genetically engineered drugs that enhance or impair endocrine, metabolic, and immune parameters and functions. Topics related to the neuroendocrine-immune axis are given special emphasis in view of the growing interest in stress-related, inflammatory, autoimmune, and degenerative disorders.
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