脱氢表雄酮与额部纤维性脱发：分子及生理病理机制
DHEA and frontal fibrosing alopecia: molecular and physiopathological mechanisms.
作者信息
Gaspar Neide Kalil
机构信息
Universidade Federal Fluminense (UFF) - Niterói (RJ), Brazil.
出版信息
An Bras Dermatol. 2016 Nov-Dec;91(6):776-780. doi: 10.1590/abd1806-4841.20165029.
Abstract
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.
摘要
转化生长因子-β1（TGFβ1）可促进纤维化，使上皮细胞和静止的成纤维细胞分化为肌成纤维细胞，并增加细胞外基质的表达。最近的研究表明，过氧化物酶体增殖物激活受体（PPAR*）是TGFβ1诱导的纤维化事件的负调节因子。脱氢表雄酮（DHEA）是一种对PPAR功能至关重要的免疫调节激素，在一些以纤维化为特征的过程中会减少。尽管瘢痕性脱发通常发生在女性的生理时期，此时DHEA的产生会减少，但文献中没有关于其减少与这种疾病的纤维化过程之间关系的数据。本文旨在综述TGFβ1的纤维化活性、其受PPAR的调控以及它与额部纤维化性脱发中DHEA的关系。
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