ArticleInvestigative ophthalmology & visual science2025
Recombinant Thrombomodulin Domain 1 Modulates Macrophage Polarization and Enhances Healing in Corneal Alkali Burns.
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 4 papers.
What it found
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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.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Delivery of Anti-VEGFA Antibody by Plant-Derived Exosome-like Nanovesicles Alleviates Corneal Angiogenesis and Fibrosis via Topical Ocular Administration.Molecules (Basel, Switzerland) · 2026Article
- AIF-1 Drives Corneal Neovascularization by Promoting Inflammatory Macrophage Activation via the MAPK and PI3K/AKT/mTOR Signaling Pathways.Investigative ophthalmology & visual science · 2026Article
- Recombinant Thrombomodulin Domain 1 Promotes Diabetic Corneal Wound Healing by Inhibiting HMGB1 Production and NLRP3 Inflammasome.Mediators of inflammation · 2026Article
- Rapamycin Mitigates Corneal Damage in a Mouse Model of Alkali Burn Injury.Bioengineering (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Corneal alkali burns are severe ocular injuries characterized by intense inflammation, tissue damage, and vision impairment, with current treatments often insufficient in restoring corneal function and clarity. This study aimed to evaluate the therapeutic effects of recombinant thrombomodulin domain 1 (rTMD1) in the treatment of corneal alkali burns, focusing on its impact on inflammation, tissue repair, fibrosis, and neovascularization. Methods: A murine model of corneal alkali burn was utilized to investigate the therapeutic potential of rTMD1. The effects of rTMD1 on macrophage polarization, inflammatory response, tissue repair, fibrosis, and neovascularization were assessed through histological analysis, immunohistochemistry, and molecular studies targeting key signaling pathways such as ERK/HIF-1α and vascular endothelial growth factor (VEGF) expression. Results: Administration of rTMD1 significantly modulated macrophage polarization, promoting a transition from the pro-inflammatory M1 phenotype to the reparative M2 phenotype via inhibition of the ERK/HIF-1α pathway. This shift resulted in reduced inflammation, enhanced tissue repair, and controlled fibrosis. Furthermore, rTMD1 inhibited neovascularization by downregulating VEGF expression, aiding in the preservation of corneal clarity. Conclusions: rTMD1 demonstrates substantial therapeutic potential in treating corneal alkali burns by reducing inflammation, promoting tissue repair, controlling fibrosis, and inhibiting neovascularization. These findings support the further development of rTMD1 as a promising treatment for corneal burns and possibly other inflammatory ocular conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.