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DHEA and frontal fibrosing alopecia: molecular and physiopathological mechanisms
The transforming growth factor-beta 1 (TGFβ1) promotes fibrosis, differentiating epithelial cells and quiescent fibroblasts into myofibroblasts and increasing expression of extracellular matrix. Recent investigations have shown that PPAR (peroxisome proliferator-activated receptor*) is a negative re...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Sociedade Brasileira de Dermatologia
2016
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5193189/ https://www.ncbi.nlm.nih.gov/pubmed/28099600 http://dx.doi.org/10.1590/abd1806-4841.20165029 |
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author | Gaspar, Neide Kalil |
author_facet | Gaspar, Neide Kalil |
author_sort | Gaspar, Neide Kalil |
collection | PubMed |
description | The transforming growth factor-beta 1 (TGFβ1) promotes fibrosis, differentiating epithelial cells and quiescent fibroblasts into myofibroblasts and increasing expression of extracellular matrix. Recent investigations have shown that PPAR (peroxisome proliferator-activated receptor*) is a negative regulator of fibrotic events induced by TGFβ1. Dehydroepiandrosterone (DHEA) is an immunomodulatory hormone essential for PPAR functions, and is reduced in some processes characterized by fibrosis. Although scarring alopecia characteristically develops in the female biological period in which occurs decreased production of DHEA, there are no data in the literature relating its reduction to fibrogenic process of this condition. This article aims to review the fibrogenic activity of TGFβ1, its control by PPAR and its relation with DHEA in the frontal fibrosing alopecia. |
format | Online Article Text |
id | pubmed-5193189 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Sociedade Brasileira de Dermatologia |
record_format | MEDLINE/PubMed |
spelling | pubmed-51931892016-12-29 DHEA and frontal fibrosing alopecia: molecular and physiopathological mechanisms Gaspar, Neide Kalil An Bras Dermatol Review The transforming growth factor-beta 1 (TGFβ1) promotes fibrosis, differentiating epithelial cells and quiescent fibroblasts into myofibroblasts and increasing expression of extracellular matrix. Recent investigations have shown that PPAR (peroxisome proliferator-activated receptor*) is a negative regulator of fibrotic events induced by TGFβ1. Dehydroepiandrosterone (DHEA) is an immunomodulatory hormone essential for PPAR functions, and is reduced in some processes characterized by fibrosis. Although scarring alopecia characteristically develops in the female biological period in which occurs decreased production of DHEA, there are no data in the literature relating its reduction to fibrogenic process of this condition. This article aims to review the fibrogenic activity of TGFβ1, its control by PPAR and its relation with DHEA in the frontal fibrosing alopecia. Sociedade Brasileira de Dermatologia 2016 /pmc/articles/PMC5193189/ /pubmed/28099600 http://dx.doi.org/10.1590/abd1806-4841.20165029 Text en http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Gaspar, Neide Kalil DHEA and frontal fibrosing alopecia: molecular and physiopathological mechanisms |
title | DHEA and frontal fibrosing alopecia: molecular and physiopathological
mechanisms |
title_full | DHEA and frontal fibrosing alopecia: molecular and physiopathological
mechanisms |
title_fullStr | DHEA and frontal fibrosing alopecia: molecular and physiopathological
mechanisms |
title_full_unstemmed | DHEA and frontal fibrosing alopecia: molecular and physiopathological
mechanisms |
title_short | DHEA and frontal fibrosing alopecia: molecular and physiopathological
mechanisms |
title_sort | dhea and frontal fibrosing alopecia: molecular and physiopathological
mechanisms |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5193189/ https://www.ncbi.nlm.nih.gov/pubmed/28099600 http://dx.doi.org/10.1590/abd1806-4841.20165029 |
work_keys_str_mv | AT gasparneidekalil dheaandfrontalfibrosingalopeciamolecularandphysiopathologicalmechanisms |