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PPAR Research
Volume 2015, Article ID 124624, 12 pages
Review Article

The Role of PPAR Gamma in Systemic Sclerosis

1Serviço de Reumatologia do Hospital das Clínicas da Universidade Federal de Pernambuco (HC-UFPE), 50670-901 Recife, PE, Brazil
2Laboratório de Imunomodulação e Novas Abordagens Terapêuticas da Universidade Federal de Pernambuco (LINAT-UFPE), 50670-901 Recife, PE, Brazil
3Laboratório de Planejamento e Síntese de Fármacos da Universidade Federal de Pernambuco (LPSF-UFPE), 50670-901 Recife, PE, Brazil

Received 11 February 2015; Revised 23 April 2015; Accepted 23 April 2015

Academic Editor: Tom Hsun-Wei Huang

Copyright © 2015 Andréa Tavares Dantas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Fibrosis is recognized as an important feature of many chronic diseases, such as systemic sclerosis (SSc), an autoimmune disease of unknown etiology, characterized by immune dysregulation and vascular injury, followed by progressive fibrosis affecting the skin and multiple internal organs. SSc has a poor prognosis because no therapy has been shown to reverse or arrest the progression of fibrosis, representing a major unmet medical need. Recently, antifibrotic effects of PPARγ ligands have been studied in vitro and in vivo and some theories have emerged leading to new insights. Aberrant PPARγ function seems to be implicated in pathological fibrosis in the skin and lungs. This antifibrotic effect is mainly related to the inhibition of TGF-β/Smad signal transduction but other pathways can be involved. This review focused on recent studies that identified PPARγ as an important novel pathway with critical roles in regulating connective tissue homeostasis, with emphasis on skin and lung fibrosis and its role on systemic sclerosis.