ArticleInvestigative ophthalmology & visual science2025
Somatostatin Ameliorates Corneal Nerve Abnormalities and Inflammation Through Regulation of Macrophage Activities in Dry Eye Disease.
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 1 paper.
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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
1 citing paper in PubMed.
- Endogenous Therapeutic Agents for Acute Corneal and Ocular Surface Injuries.Translational vision science & technology · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This study aimed to investigate the therapeutic effects of pasireotide (SOM230) on corneal nerve abnormalities in a mouse model of dry eye disease (DED) and to elucidate its potential mechanisms of action. Methods: Male C57BL/6J mice underwent lacrimal gland excision (LGE) to induce DED and were treated with SOM230 or PBS. Corneal epithelial integrity, pain-related behaviors, and corneal sensitivity were evaluated. RNA sequencing was performed to identify potential pathways modulated by SOM230. Flow cytometry and immunofluorescence quantified macrophage polarization states. Results: SOM230 treatment significantly improved corneal epithelial integrity, reduced pain behaviors, and restored corneal sensitivity compared to PBS. RNA sequencing revealed that SOM230 downregulated key inflammatory pathways, including TNF-α and NF-κB. Flow cytometry and immunofluorescence showed that SOM230 modulated macrophage polarization by decreasing pro-inflammatory M1 macrophages and enhancing anti-inflammatory M2 macrophages, contributing to reduced corneal inflammation and improved healing. Conclusions: SOM230 alleviates nerve abnormalities in DED by suppressing inflammatory pathways (TNF-α, NF-κB) and promoting a shift in macrophage polarization from the pro-inflammatory M1 phenotype to the reparative M2 phenotype. These findings suggest that modulation of macrophage polarization is a crucial mechanism underlying the therapeutic effects of SOM230, highlighting its potential as a treatment strategy for nerve damage in DED.
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