ArticleScientific reports2016
ITF2357 transactivates Id3 and regulate TGFβ/BMP7 signaling pathways to attenuate corneal fibrosis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 45 citations in OpenAlex.
- Comparison of tear proteomic and neuromediator profiles changes between small incision lenticule extraction (SMILE) and femtosecond laser-assisted in-situ keratomileusis (LASIK).Journal of advanced research · 2021Trial
- ITF2357 exerts anti‑tumor activity in colorectal cancer via the miR‑1938/ADAM12 axis.Molecular biology reports · 2026Article
- The Role of Epigenetics in Corneal Fibrosis.Epigenomes · 2026Review
- Article
- Single-Cell Transcriptomics Reveals a Multi-Compartmental Cellular Cascade Underlying Elahere-Induced Ocular Toxicity in Rats.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Bone morphogenetic proteins (BMPs) at the forefront of ocular diseases and therapeutics.Eye and vision (London, England) · 2025Review
- Use of femtosecond laser generated reactive oxygen species to manage inflammation and enhance wound healing after ocular trauma.Scientific reports · 2025Article
- Inhibitor of DNA-Binding 3 Is a Novel Regulator of Limbal Epithelial Cell Migration Via the EphA2/Akt Signaling Pathway.Investigative ophthalmology & visual science · 2025Article
- PI3K signaling and lysyl oxidase is critical to corneal stroma fibrosis following mustard gas injury.Experimental eye research · 2025Article
- ITF2357 regulates NF-κB signaling pathway to protect barrier integrity in retinal pigment epithelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Potential therapeutic effects of peroxisome proliferator-activated receptors on corneal diseases.Experimental biology and medicine (Maywood, N.J.) · 2024Review
- Mustard Gas Exposure Actuates SMAD2/3 Signaling to Promote Myofibroblast Generation in the Cornea.Cells · 2023Article
- Review
- Corneal stromal repair and regeneration.Progress in retinal and eye research · 2022Review
- Corneal fibrosis abrogation by a localized AAV-mediated inhibitor of differentiation 3 (Id3) gene therapy in rabbit eyes in vivo.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- BMP3 inhibits TGFβ2-mediated myofibroblast differentiation during wound healing of the embryonic cornea.NPJ Regenerative medicine · 2022Article
- Evaluation of a novel combination of TRAM-34 and ascorbic acid for the treatment of corneal fibrosis in vivo.PloS one · 2022Article
- Corneal neuromediator profiles following laser refractive surgery.Neural regeneration research · 2021Review
- ID1 and ID3 are Negative Regulators of TGFβ2-Induced Ocular Hypertension and Compromised Aqueous Humor Outflow Facility in Mice.Investigative ophthalmology & visual science · 2021Article
- Glutathione is a potential therapeutic target for acrolein toxicity in the cornea.Toxicology letters · 2021Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
Abstract
Corneal fibrosis is often seen in patients with ocular trauma and infection that compromises corneal transparency resulting in vision loss. Treatment strategies including NSAIDs, steroids, MMC and corneal transplants have shown tremendous success but with several side effects and cellular toxicity. Histone deacetylase inhibitors (HDACi) have been shown to inhibit corneal fibrosis via TGFβ signaling pathway. In this study, we investigated safety, efficacy and mechanism of action of a HDACi, ITF2357 in TGFβ-stimulated in vitro primary human cornea stromal fibroblasts (pHCSFs) and in vivo in a photorefractive keratectomy-treated rabbit model of corneal fibrosis. We found that in vivo ITF2357 decreased collagen I, collagen IV, fibronectin, integrin αVβ3 expression with a reduction in corneal haze. In addition, ITF2357 reduced myofibroblast formation, suppressed phosphorylation of Smad proteins in TGFβ pathway and inhibited key responsive protein, P4HA1 involved in pro-collagen synthesis. Treatment of pHCSFs with ITF2357 activated BMP7 levels and expressed all the members of inhibitor of differentiation proteins (Id1-Id4), however, it failed to rescue TGFβ-driven transdifferentiation of fibroblasts to myofibroblasts in the presence of siRNA specific to Id3. We conclude that ITF2357 is a potential anti-fibrotic drug that exerts its action via activation of Id3, a downstream target of TGFβ/BMP7 signaling pathways.
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