Evidence map›Paper›PMID 42417589›Full record

ArticleInvestigative ophthalmology & visual science2026

Ocular IL-1α/IFN-γ Delay the Corneal Wound Healing in Rheumatoid Arthritis Through Mitochondrial Dysfunction and NLRP3 Inflammasome Activation.

Zhiwei Ren, Dingwen Cao, Jiayu Meng, Yanling Dong, Lei Xu, Liuli Wang, Chao Wei, Jiang Bian

Abstract read
In one paragraph

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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Zhiwei RenState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Dingwen CaoState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Jiayu MengState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Yanling DongState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Lei XuState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Liuli WangState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Chao WeiState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Jiang BianState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Rheumatoid arthritis (RA) is an autoimmune disease often associated with corneal ulceration and impaired corneal epithelial wound healing (CEWH), although the underlying cause remains unclear. This study aims to elucidate the pathogenic mechanism of RA-associated delayed CEWH. Methods: We integrated analyses of human clinical samples, a murine collagen-induced arthritis (CIA) model, a human corneal epithelial cell (HCEC) culture platform, as well as Olink proteomic and transcriptomic analysis. We characterized RA-related ocular phenotypes, evaluated the effects of IL-1α/IFN-γ on HCECs, and validated interventions using the NLRP3 inflammasome inhibitor MCC950. Results: RA patients exhibited delayed CEWH, reduced tear secretion, and heightened ocular surface inflammation characterized by elevated Oncostatin M (OSM), IL-1α and IFN-γ. OSM alone promoted the proliferation and migration of HCECs and enhanced mitochondrial respiratory capacity. However, these beneficial effects were markedly impaired when OSM-treated HCECs were co-exposed to IL-1α and IFN-γ, an effect accompanied by severe mitochondrial damage, compromised oxidative phosphorylation, and increased NLRP3 inflammasome activity. Notably, pharmacological blockade of NLRP3 inflammasome with MCC950 significantly restored HCEC functions compromised by IL-1α/IFN-γ exposure, with improved mitochondrial ultrastructure and function. Furthermore, topical MCC950 administration accelerated CEWH in the CIA model. Conclusions: Ocular IL-1α/IFN-γ impairs corneal epithelial function by disrupting mitochondrial integrity and amplifying NLRP3-mediated inflammatory cascades, thereby contributing to delayed CEWH in RA patients.

Indexed as

Arthritis, RheumatoidInflammasomesInterferon-gammaInterleukin-1alphaMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinWound HealingAnimalsCells, CulturedDisease Models, AnimalEpithelium, CornealFemaleHumansMaleMiceMice, Inbred C57BLInflammasomesInterferon-gammaInterleukin-1alphaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID42417589
PMCPMC13355393

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Registered trials

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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.