dc.contributorUniversidade Estadual Paulista (UNESP)
dc.contributorUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2022-11-30T13:45:12Z
dc.date.accessioned2022-12-20T14:50:49Z
dc.date.available2022-11-30T13:45:12Z
dc.date.available2022-12-20T14:50:49Z
dc.date.created2022-11-30T13:45:12Z
dc.date.issued2022-07-29
dc.identifierDermatology And Therapy. Northcote: Adis Int Ltd, v. 12, n. 9, p. 1967-1988, 2022.
dc.identifier2193-8210
dc.identifierhttp://hdl.handle.net/11449/237796
dc.identifier10.1007/s13555-022-00779-x
dc.identifierWOS:000832846100001
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/5417852
dc.description.abstractMelasma is a multifactorial dyschromia that results from exposure to external factors (such as solar radiation) and hormonal factors (such as sex hormones and pregnancy), as well as skin inflammation (such as contact dermatitis and esthetic procedures), in genetically predisposed individuals. Beyond hyperfunctional melanocytes, skin with melasma exhibits a series of structural and functional alterations in the epidermis, basement membrane, and upper dermis that interact to elicit and sustain a focal hypermelanogenic phenotype. Evolution in the knowledge of the genetic basis of melasma and the cutaneous response to solar radiation, as well as the roles of endocrine factors, antioxidant system, endothelium proliferation, fibroblast senescence, mast cell degranulation, autophagy deficits of the melanocyte, and the paracrine regulation of melanogenesis, will lead to the development of new treatments and preventive strategies. This review presents current knowledge on these aspects of the pathogenesis of melasma and discusses the effects of specific treatments and future research on these issues.
dc.languageeng
dc.publisherAdis Int Ltd
dc.relationDermatology And Therapy
dc.sourceWeb of Science
dc.subjectMelasma
dc.subjectPathogenesis
dc.subjectMelanocytes
dc.subjectMelanin
dc.subjectPhotoaging
dc.subjectUV radiation
dc.titleUpdate on Melasma-Part I: Pathogenesis
dc.typeOtros


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