Abstract

Background: The expression of biological mediators, such as growth factors and cytokines, after skin damage, and their balance, is important to guarantee proliferation, differentiation and migration of cells and extracellular matrix, as well as to the homeostasis during tissue remodeling. The present review means to clarify their functions over inflammation, proliferation and remodeling stages of skin regeneration. Methods: Reviews, experimental studies and clinical trials included in this paper were search on PubMed database using the following terms: platelet-derived growth factor, interleukin 1, tumor necrosis factor alpha, keratinocyte growth factor, transforming growth factor beta, endothelial vascular growth factor, matrix metalloproteinase 9, tissue metalloproteinase inhibitor 1, interferon gamma, transcription nuclear factor kappa B, skin inflammation, skin cell proliferation, skin extracellular matrix and skin regeneration. Results and Discussion: Several studies on the signaling mechanism of these mediators in normal and impaired healing have already been developed and have shown promising results. Currently, some of these mediators are already direct focuses of potential clinical therapies that address the treatment of acute and chronic skin wounds. These mediators, basically synthetized by platelets, macrophages, vascular endothelial cells, fibroblasts and keratinocytes, act on epidermis and dermis proliferation, hypertrophy and cell migration, resulting in formation of granulation tissue, reepithelization and extracellular matrix remodeling and angiogenesis. A better understanding of the action of these mediators can provide greater knowledge not only of their roles in the natural healing process but also in the presence of disorders that affect skin repair. Conclusion: Future studies aimed to understand the mechanism of action of these mediators in the different types of cells involved in wound healing may lead to the discovery of new therapeutics to optimize the treatment of skin pathologies.

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