ArticleInvestigative ophthalmology & visual science2025
Epigenetic Reprogramming Via Sodium Butyrate Induces Corneal Myofibroblast Dedifferentiation In Vitro and Inhibits Fibrosis In Vivo.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The Role of Epigenetics in Corneal Fibrosis.Epigenomes · 2026Review
- Myogenic Differentiation (MyoD) Gene Expression in Cornea and Role in Corneal Myofibroblast Dedifferentiation.Investigative ophthalmology & visual science · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
Purpose: Abnormal corneal myofibroblast (CMF) differentiation and persistence in stroma after ocular trauma causes corneal fibrosis and impaired vision. This study tested whether epigenetic reprogramming via sodium butyrate (NaB), histone deacetylase inhibitor, could provoke CMF dedifferentiation into precursor/non-opaque corneal fibroblast/keratocyte (CSF) like cells using human in vitro and rabbit in vivo corneal fibrosis models. Methods: Healthy human cadaver corneas generated CSFs were converted into CMFs by TGFβ1 (5ng/ml) and grown in -/+ NaB (5 mM) for 72 hours. Quantitative RT-PCR and immunofluorescence measured changes in profibrotic markers (alpha smooth muscle actin [αSMA], collagen-III [Col-III], fibronectin [FN]) and fibroblast marker (fibroblast-specific protein-1 [FSP1]). Epigenetic reprogramming was measured by quantification of total HDAC activity by commercial-kit and DNA methylation using methylation-specific PCR primers for αSMA, Col-III, and FSP1 genes. Collagen gel contraction assay (CGA) evaluated response of NaB on CMF's contractile function. In vivo clinical utility of NaB in reducing corneal fibrosis was evaluated via stereomicroscopy and Pentacam imaging in live rabbits. Results: NaB treatment to CMFs changed myofibroblast-morphology to fibroblast-like and significantly reduced αSMA (P = 0.0005), Col-III (P = 0.011), FN (P = 0.0004), and increased FSP1 (P = 0.0004) gene expression in human in vitro. Additionally, it significantly reduced total HDAC activity (P = 0.0009) with hypermethylation of αSMA, Col-III, and hypomethylation of FSP1 gene promoters. Also, NaB-treated CMFs showed significantly reduced contractility (P < 0.0001) in CGA. Topical NaB treatment markedly reduced opacity in alkali-injured rabbit corneas in vivo. Conclusions: Dedifferentiation of CMFs via epigenetic reprogramming by NaB offers an attractive approach to treat corneal fibrosis in vivo. Additional studies are warranted.
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Registered trials
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