ArticleInvestigative ophthalmology & visual science2026
Corneal Nerves Promote Alkali Burn Repair by Modulating Macrophages and Neutrophils via Calcitonin Gene-Related Peptide.
Article in Investigative ophthalmology & visual science, 2026. 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.
- Article
- CGRP: the immune system's double agent - context-dependent roles in inflammation, resolution and cancer.Frontiers in immunology · 2026Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This study aims to investigate the role of calcitonin gene-related peptide (CGRP) in corneal tissue repair in alkali burn and its underlying neuro-immune mechanisms. Methods: Mouse corneal nerves were ablated via surgery or resiniferatoxin (RTX) to study their role in tissue healing after an alkali burn. CGRP and its receptor levels were quantified by Western blot and quantitative PCR (qPCR). Alkali-burned corneas were treated topically with CGRP or BIBN-4096. Tissue repair, inflammatory cytokine expression, and immune cell infiltration were subsequently assessed. Macrophages were depleted using PLX5622 to evaluate their effect on healing. Furthermore, mouse macrophages and neutrophils were cultured in vitro, and transcriptomic analysis was performed to elucidate functional and molecular alterations, which were validated experimentally. Results: Corneal nerve ablation significantly delayed corneal alkali burns healing. In alkali burns, corneal nerves released CGRP, leading to elevated CGRP levels in the cornea. Topical CGRP application promoted tissue repair and reduced inflammation, whereas its antagonist BIBN-4096 impeded healing. Macrophage depletion not only delayed repair but also abolished the therapeutic effect of CGRP, indicating that macrophages are crucial for CGRP-mediated repair. Mechanistically, CGRP promoted neutrophil apoptosis and enhanced macrophage apoptosis, efferocytosis, and anti-inflammatory functions via the cAMP-TSP-1 pathway, thereby facilitating tissue repair. Conclusions: This study reveals that in corneal alkali burns, corneal nerves promote tissue repair by secreting CGRP to regulate neuro-immune interactions, providing new insights for the treatment of corneal alkali burns.
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Registered trials
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