A PPAR-Gamma Agonist Rosiglitazone Suppresses Fibrotic Response in Human Pterygium Fibroblasts by Modulating the p38 MAPK Pathway | Zendy

Selikem Abla Nuwormegbe | Zendy; Joon Hyung Sohn | Zendy; Sun Woong Kim | Zendy

Open Access

A PPAR-Gamma Agonist Rosiglitazone Suppresses Fibrotic Response in Human Pterygium Fibroblasts by Modulating the p38 MAPK Pathway

Author(s) -

Selikem Abla Nuwormegbe,

Joon Hyung Sohn,

Sun Woong Kim

Publication year - 2017

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.17-22203

Subject(s) - rosiglitazone , peroxisome proliferator activated receptor , endocrinology , medicine , mapk/erk pathway , signal transduction , chemistry , receptor , transforming growth factor , viability assay , agonist , fibrosis , cancer research , fibronectin , fibroblast , blot , microbiology and biotechnology , biology , apoptosis , cell , in vitro , biochemistry , gene

Fibroblast activation may play an important role in pterygium progression. Synthetic peroxisome proliferator-activated receptor γ (PPAR-γ) ligands have been shown to be effective antifibrotic agents against transforming growth factor β1 (TGF-β1) induced fibrosis in several tissues. We aimed to investigate the antifibrotic effects of the PPAR-γ ligand rosiglitazone in pterygium fibroblasts and the underlying mechanisms.

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