Evidence map›Paper›PMID 41247402›Full record

ArticleActa diabetologica2026

METTL14-dependent regulation of HMGB1 attenuates inflammation in diabetic retinopathy.

Zhangxin Huang, Jitian Guan, Xue Zhang, Qiang Hu, Jiayang Huang, Wei Sang, Xiaoning Wang, Bo Jiang, Dawei Sun

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Article in Acta diabetologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
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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

9 authors.

Zhangxin HuangDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Jitian GuanDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Xue ZhangDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Qiang HuDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Jiayang HuangDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Wei SangDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Xiaoning WangDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Bo JiangDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Dawei SunDepartment of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China. sundawei@hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-9717-0190

Funding

National Natural Science Foundation of China 82171103National Natural Science Foundation of China U23A20389
6 · The paper itself

Abstract

backgroundDiabetic retinopathy (DR) is a frequent complication of diabetes, characterized by progressive vision loss, with chronic inflammation being an important contributor in its development. N6-methyladenine (m6A) is a crucial RNA modification within eukaryotes, playing an essential role in different bodily functions and disease states. Nonetheless, the precise mechanism underlying m6A modification in DR remains elusive.

methodsBV2 cells were stimulated with high glucose (HG) and mice were injected intraperitoneally with streptozotocin (STZ) to induce inflammation. RT-qPCR, Western blot, ELISA, immunofluorescence, CCK-8, Wound Healing, and RIP assays were used to evaluate the effects of methyltransferase-like 14 (METTL14) in these models.

resultsOur study indicated significantly decreased levels of METTL14 in HG stimulated BV2 cells and in STZ models. In addition, METTL14 levels were reduced in peripheral venous samples of DR patients. Meanwhile, the inflammatory factors were inhibited by up-regulation of METTL14 in HG stimulated BV2 cells and STZ models. Mechanistically, METTL14 overexpression inhibited high mobility group box 1 (HMGB1), thereby suppressing nuclear factor kappa-B (NF-κB) signaling pathway activation.

conclusionThis study suggested that METTL14 may influence inflammation in DR by modulating the HMGB1/NF-κB pathway, providing valuable insights into potential therapeutic approaches for DR.

Indexed as

Diabetic RetinopathyHMGB1 ProteinInflammationMethyltransferasesAnimalsCell LineDiabetes Mellitus, ExperimentalHumansMaleMiceMice, Inbred C57BLNF-kappa BSignal TransductionHMGB1 ProteinHMGB1 protein, mouseMethyltransferasesMETTL14 protein, humanNF-kappa BDiabetic retinopathyHigh mobility group protein 1Inflammationm6A modificationMethyltransferase-like 14

Identifiers

PMID41247402

What Socratic holds

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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 Socratic graph.