alexa Peroxisome Proliferator-Activated Receptor Gamma (PPAR-Γ) Agonist Troglitazone Suppresses Collagen Synthesis via Expression of the Downstream Target Mirnas: A Novel Strategy to Treat Skin Fibrosis?
ISSN: 2167-7700

Chemotherapy: Open Access
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Commentary

Peroxisome Proliferator-Activated Receptor Gamma (PPAR-Γ) Agonist Troglitazone Suppresses Collagen Synthesis via Expression of the Downstream Target Mirnas: A Novel Strategy to Treat Skin Fibrosis?

Hua-yu Zhu1, Wen-dong Bai2, Hong-tao Wang1, Jun-tao Han1 and Da-hai Hu1*

1Department of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University, Xi’an, Shaanxi, P.R China

2Department of Clinical Laboratory Center, Xinjiang Command General Hospital of Chinese People’s Liberation Army, Urumqi, Xinjiang, P.R China

Corresponding Author:
Da-hai Hu
Department of Burns and Cutaneous Surgery
Xijing Hospital, Fourth Military Medical University
Xi’an, Shaanxi, P.R China
Tel: +86-29-84775293
E-mail: [email protected]

Received Date: August 05, 2016; Accepted Date: October 24, 2016; Published Date: October 29, 2016

Citation: Zhu HY, Bai WD, Wang HT, Han JT, Hu DH (2016) Peroxisome Proliferator-Activated Receptor Gamma (PPAR-Γ) Agonist Troglitazone Suppresses Collagen Synthesis via Expression of the Downstream Target Mirnas: A Novel Strategy to Treat Skin Fibrosis? Chemo Open Access 5:218. doi: 10.4172/2167-7700.1000218

Copyright: © 2016 Da-hai Hu, et al. 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 author and source are credited.

Abstract

Nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ) activity has been identified as an important endogenous anti-fibrotic defense mechanism. Troglitazone, a PPAR-γ agonist, has been used to suppress the formation of keloids and growth of hypertrophic scar fibroblasts. Indeed, the PPAR-γ agonist was able to inhibit collagen I expression in hypertrophic scar fibroblasts, which clearly demonstrates its therapeutic potential, and clarification of the underlying molecular mechanisms could further indicate the usefulness of the PPAR-γ agonists in the treatment of keloids. Moreover, increasing evidence has suggested that aberrant expression of miRNAs leads to the development and progression of fibrosis diseases. Thus, fully understanding the biological functions and molecular mechanisms of miRNAs in the regulation of fibrosis could provide insight for advancements in the diagnosis and treatment of fibrosis. This commentary briefly summarizes the current evidence for the ability of PPAR-γ agonist troglitazone to suppress collagen synthesis and regulate miRNA expression and downstream targets in cells.

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