Entropy
Member
- Joined
- Apr 11, 2015
- Messages
- 163
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.
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The importance of the effect of DHEA on mitochondrial oxidative metabolism was stabilished by administration of this hormone in rats. These animals showed increased liver and brain metabolism with elevated brain weight without concurrent increase in body weight.52 The results observed in the topographic response is demonstrative of the variation in distribution of DHEA receptors in the body of these animals.
Tests with radioactive DHEA administered to dogs confirmed their higher metabolism in fibroblasts derived from dermal follicles and, among these, in dermal fibroblasts derived from the follicles of the skulls of the animals, accentuating the topographic differences of their receptors.53
The relation between the activity of DHEA and FFA is also suggested by the reduction of DHEA levels in different conditions characterized by fibrosis, such as occurs in idiopathic pulmonary fibrosis.47 A comparison of the serum levels of DHEA/DHEAS of 137 patients with idiopathic pulmonary fibrosis and 58 controls showed a significant reduction of these hormones in patients, both in plasma and in the bronchoalveolar lavage fluid.
CONCLUSIONS
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 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.
-
The importance of the effect of DHEA on mitochondrial oxidative metabolism was stabilished by administration of this hormone in rats. These animals showed increased liver and brain metabolism with elevated brain weight without concurrent increase in body weight.52 The results observed in the topographic response is demonstrative of the variation in distribution of DHEA receptors in the body of these animals.
Tests with radioactive DHEA administered to dogs confirmed their higher metabolism in fibroblasts derived from dermal follicles and, among these, in dermal fibroblasts derived from the follicles of the skulls of the animals, accentuating the topographic differences of their receptors.53
The relation between the activity of DHEA and FFA is also suggested by the reduction of DHEA levels in different conditions characterized by fibrosis, such as occurs in idiopathic pulmonary fibrosis.47 A comparison of the serum levels of DHEA/DHEAS of 137 patients with idiopathic pulmonary fibrosis and 58 controls showed a significant reduction of these hormones in patients, both in plasma and in the bronchoalveolar lavage fluid.
CONCLUSIONS
- PPARγ is the main regulator of lipid cell metabolism and sebocytes development. The reduction of its activity is responsible for fibrosis;
- DHEA is an important stimulator of PPARs;
- Reduction of DHEA is observable in some diseases characterized by fibrosis;
- Frontal fibrogenic alopecia typically develops in the woman life period in which production of DHEA is decreased;
- It is possible that the reduction of the local activity of DHEA is responsible for follicular fibrogenic process of this alopecia;
- It is also possible that the better understanding on the variation of topography dynamic of tissue activity of DHEA changes therapeutic strategies in other conditions characterized by fibrosis.
DHEA and frontal fibrosing alopecia: molecular and physiopathological mechanisms