ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2022
Lobeglitazone attenuates fibrosis in corneal fibroblasts by interrupting TGF-beta-mediated Smad signaling.
Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- The Mechanistic Role of PPARPPAR research · 2026Review
- S1P, Generated by Sphingosine Kinase 1, Negatively Affects Corneal Wound Healing Process by Activating TGF-β/Smad Pathway.Analytical cellular pathology (Amsterdam) · 2026Article
- Review
- Amelioration of Fibrosis via S1P Inhibition Is Regulated by Inactivation of TGF-β and SPL Pathways in the Human Cornea.International journal of molecular sciences · 2024Article
- Potential therapeutic effects of peroxisome proliferator-activated receptors on corneal diseases.Experimental biology and medicine (Maywood, N.J.) · 2024Review
- Review
- Novel Correlation between TGF-β1/-β3 and Hormone Receptors in the Human Corneal Stroma.International journal of molecular sciences · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeTransforming growth factor beta 1 (TGF-β1) is an important cytokine released after ocular surface injury to promote wound healing. However, its persistence at the injury site triggers a fibrotic response that leads to corneal scarring and opacity. Thiazolidinediones (TZDs) are synthetic peroxisome proliferator-activated receptor gamma (PPAR-γ) ligands used to regulate glucose and lipid metabolism in the management of type 2 diabetes. Studies have also showed TZDs have antifibrotic effect. In this study, we investigated the antifibrotic effect of the TZD lobeglitazone on TGF-β1-induced fibrosis in corneal fibroblasts.
methodsHuman primary corneal fibroblasts were cultivated and treated with TGF-β1 (5 ng/mL) to induce fibrosis, with or without pre-treatments with different concentrations of lobeglitazone. Myofibroblast differentiation and extracellular matrix (ECM) protein expression was evaluated by western blotting, immunofluorescence, real-time PCR, and collagen gel contraction assay. The effect of lobeglitazone on TGF-β1-induced reactive oxygen species (ROS) generation was evaluated by DCFDA-cellular ROS detection assay kit. Signaling proteins were evaluated by western blotting to determine the mechanism underlying the antifibrotic effect.
resultsOur results showed lobeglitazone attenuated TGF-β1-induced ECM synthesis and myofibroblast differentiation of corneal fibroblasts. This antifibrotic effect appeared to be independent of PPAR signaling and rather due to the inhibition of the TGF-β1-induced Smad signaling. Lobeglitazone also blocked TGF-β1-induced ROS generation and nicotinamide adenine dinucleotide phosphate oxidase (Nox) 4 transcription.
conclusionThese findings indicate that lobeglitazone may be a promising therapeutic agent for corneal scarring. KEY MESSAGES.
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