Evidence map›Paper›PMID 41718657›Full record

ArticleInvestigative ophthalmology & visual science2026

Advanced Glycation End-Products Contribute to Delayed Diabetic Corneal Epithelial Wound Healing via the TLR4 Signaling.

Yaoyao Yu, Yani Zhang, Yang Tang, Li Ma, Chao Wei, Xiaofei Bai

Abstract read
PubMed Full text at PMC Publisher
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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Mogroside V Alleviates Renal Injury in Diabetic Mice via Regulation of theInternational journal of molecular sciences · 2026
    Article
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

6 authors.

Yaoyao YuState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Yani ZhangState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Yang TangState Key Laboratory Cultivation Base, Shandong Key Laboratory of Eye Diseases, Eye Institute of Shandong First Medical University, Shandong First Medical University, Qingdao, China.
Li MaState 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.
Xiaofei BaiState 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: Diabetic keratopathy (DK) is a significant ocular surface complication of diabetes. This study investigated the role of advanced glycation end-products (AGEs) in DK pathogenesis and the underlying mechanism. Methods: Type I diabetes mellitus (T1DM) mouse model was established by intraperitoneal injection of streptozotocin to assess AGE accumulation and inflammatory factor expression in corneal tissues. A bone marrow-derived dendritic cell (BMDC) culture platform, RNA sequencing (RNA-seq), and pharmacological interventions were used to examine AGE-induced inflammatory response and signaling pathways. The impact of Toll-like receptor 4 (TLR4) signaling (blocked by TAK-242) and AGE formation (inhibited by pyridoxamine [PM]) on diabetic corneal epithelial wound healing (CEWH) was evaluated. Results: Compared with untreated controls, AGE-challenged BMDCs exhibited an exacerbated inflammatory response and increased phosphorylation of nuclear factor kappa-B (NF-κB) p65 and interferon regulatory factor 3 (IRF3). TLR4 blockade with TAK-242 significantly attenuated this inflammation and reduced phosphorylation of p65 and IRF3. RNA-seq analysis revealed baseline low-grade inflammation and hyper-phosphorylation of p65 and IRF3 in advanced diabetic corneas with AGE accumulation. Topical TAK-242 treatment significantly reversed delayed CEWH and accelerated corneal nerve regeneration in T1DM mice. Similarly, inhibiting AGE formation with PM also expedited diabetic CEWH and nerve regeneration. Conclusions: The AGE/TLR4 axis drives sustained corneal inflammation by activating p65 and IRF3, thereby promoting DK progression. These findings identify AGE/TLR4 signaling as a potential therapeutic target for DK.

Indexed as

Corneal DiseasesDiabetes Mellitus, ExperimentalEpithelium, CornealGlycation End Products, AdvancedToll-Like Receptor 4Wound HealingAnimalsBlotting, WesternDiabetes Mellitus, Type 1Disease Models, AnimalMaleMiceMice, Inbred C57BLSignal TransductionGlycation End Products, AdvancedTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID41718657
PMCPMC12927432

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.