DHEA and frontal fibrosing alopecia: molecular and physiopathological mechanisms.
An Bras Dermatol
; 91(6): 776-780, 2016.
Article
em En
| MEDLINE
| ID: mdl-28099600
The transforming growth factor-beta 1 (TGFß1) 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 TGFß1. 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 TGFß1, its control by PPAR and its relation with DHEA in the frontal fibrosing alopecia.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Desidroepiandrosterona
/
Alopecia
Tipo de estudo:
Etiology_studies
Limite:
Female
/
Humans
Idioma:
En
Revista:
An Bras Dermatol
Ano de publicação:
2016
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Espanha