ArticleInvestigative ophthalmology & visual science2025
RIPK3-Mediated Necroptosis Drives Macrophage Infiltration and Corneal Neovascularization After Alkali Burn.
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 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Carrier-free targeted co-assembly of glycyrrhizin and puerarin overcomes ocular barriers for corneal alkali burn therapy via macrophage reprogramming.Materials today. Bio · 2026Article
- Nintedanib Eye Drops Inhibit Alkali Burn-Induced Corneal Neovascularization Via RAP1/MEK/ERK Signaling Pathway.Investigative ophthalmology & visual science · 2026Article
- Icariin alleviates corneal neovascularization by regulating inflammation through inhibition of macrophage polarization and the NF-κB pathway.Journal of translational medicine · 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
- Emerging Roles of Regulated Cell Death-mediated Inflammation in Pathophysiology of Ocular Diseases.Journal of ophthalmic & vision research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To reveal the role of receptor-interacting protein kinase 3 (RIPK3) in regulating macrophage inflammation and corneal neovascularization (CoNV) induced by alkali burn. Methods: A corneal alkali burn (AB) model was established in C57BL/6J (wild-type) and RIPK3fl/flCx3cr1+/cre (RIPK3-/-, RIPK3 knockout [KO]) mice using sodium hydroxide. Anterior segment optical coherence tomography and hematoxylin and eosin staining were used to evaluate the impact of RIPK3 on corneal edema and morphology. CoNV was detected by slit-lamp microscopy and whole-mount immunofluorescence staining of cornea. Corneal macrophage and necroptotic cell death was analyzed through immunofluorescence staining and propidium iodide (PI) staining. Activation of the necroptosis pathway was examined after corneal AB by western blot. Results: Necroptosis-related proteins RIPK1, RIPK3, and mixed lineage kinase domain-like (MLKL) were upregulated and activated following corneal AB. Among these, RIPK3 demonstrated the most pronounced increase. Notably, the elevated level of RIPK3 was prominently colocalized with the infiltrating F4/80+ macrophages. RIPK3 KO significantly alleviated corneal edema and morphology defects. Additionally, as the corneal morphological defects progressed, macrophages became activated, and CoNV and lymphangiogenesis (LyG) were enhanced. RIPK3 KO markedly reduced AB-induced macrophage accumulation, as well as CoNV and LyG. RIPK3 KO mice also showed a meaningful decrease in PI+ necroptotic cells. Mechanistically, AB-induced necroptosis stimulated the expression of MLKL and fibroblast growth factor 2 (FGF2), whereas RIPK3 deficiency decreased their expression. Conclusions: This study revealed that RIPK3-mediated necroptosis drives macrophage inflammation and CoNV. Targeting RIPK3 could effectively suppress these responses by inhibiting the MLKL/FGF2 pathway, making it a promising therapeutic strategy for corneal AB.
Indexed as
Identifiers
What OpenQuestion holds
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.