The Role of PPAR Gamma in Systemic Sclerosis

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...

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Bibliographic Details
Published in:PPAR Research 2015-01, Vol.2015 (2015), p.4-15
Main Authors: Pitta, Maira Galdino da Rocha, Marques, Claudia Diniz Lopes, Pitta, Ivan da Rocha, da Rocha Junior, Laurindo Ferreira, Rego, Moacyr Jesus Barreto de Melo, Pereira, Michelly Cristiny, Dantas, Andréa Tavares, Duarte, Angela Luzia Branco Pinto
Format: Article
Language:English
Subjects:
Acids
Chemokines
Collagen
Cytokines
Development and progression
Disease
Extracellular matrix
Fibrosis
Gene expression
Heart attacks
Homeostasis
Kinases
Ligands
Medical prognosis
Pathogenesis
Physiological aspects
Proteins
Review
Scleroderma (Disease)
Systemic scleroderma
Transcription factors
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Summary: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.
ISSN:1687-4757
1687-4765
DOI:10.1155/2015/124624