Evidence map›Paper›PMID 38978074›Full record

ArticleBiology direct2024

YTHDC1 aggravates high glucose-induced retinal vascular endothelial cell injury via m6A modification of CDK6.

Qi Zhou, Min Tian, Yang Cao, Min Tang, Xiaohong Xiang, Lu Guo, Hongbin Lv

Abstract read
In one paragraph

Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
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  5. Article
  6. Article
  7. Article
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  9. Article
  10. Review
  11. Review
  12. Article
  13. The latest progression of N6-methyladenosine (mFrontiers in endocrinology · 2025
    Review
  14. Review
  15. Review
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

7 authors.

Qi ZhouDepartment of Ophthalmology, Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, China.
Min TianDepartment of Ophthalmology, Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, China.
Yang CaoDepartment of Ophthalmology, Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, China.
Min TangDepartment of Ophthalmology, Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, China.
Xiaohong XiangDepartment of Ophthalmology, Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, China.
Lu GuoDepartment of Ophthalmology, Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, China.
Hongbin LvDepartment of Ophthalmology, Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, 646000, China. oculistlvhongbin@swmu.edu.cn.

Funding

Luzhou Municipal People's Government-Southwest Medical University Science and Technology Strategic Cooperation Project No. 2023LZXNYDJ005Sichuan Science and Technology Program 2022YFS0611
6 · The paper itself

Abstract

objectiveRetinal vascular endothelial cell (RVECs) injury is a major cause of morbidity and mortality among the patients with diabetes. RVECs dysfunction is the predominant pathological manifestation of vascular complication in diabetic retinopathy. N6-methyladenosine (m6A) serves as the most prevalent modification in eukaryotic mRNAs. However, the role of m6A RNA modification in RVECs dysfunction is still unclear.

methodsRT-qPCR analysis and western blot were conducted to detect the change of m6A RNA modification in diabetic retinopathy. CCK-8 assay, transwell experiment, wound healing assay, tube formation experiment, m6A-IP-qPCR were performed to determine the role of YTHDC1 in RVECs. Retinal trypsin digestion test and H&E staining were used to evaluate histopathological changes.

resultsThe levels of m6A RNA methylation were significantly up-regulated in HG-induced RVECs, which were caused by increased expression of YTHDC1. YTHDC1 regulated the viability, proliferation, migration and tube formation ability in vitro. YTHDC1 overexpression impaired RVECs function by repressing CDK6 expression, which was mediated by YTHDC1-dependent mRNA decay. Moreover, it showed sh-YTHDC1 inhibited CDK6 nuclear export. Sh-YTHDC1 promotes the mRNA degradation of CDK6 in the nucleus but does not affect the cytoplasmic CDK6 mRNA. In vivo experiments showed that overexpression of CDK6 reversed the protective effect of sh-YTHDC1 on STZ-induced retinal tissue damage.

conclusionYTHDC1-mediated m6A methylation regulates diabetes-induced RVECs dysfunction. YTHDC1-CDK6 signaling axis could be therapeutically targeted for treating DR.

Indexed as

AdenosineCyclin-Dependent Kinase 6Diabetic RetinopathyEndothelial CellsGlucoseAnimalsCell ProliferationHumansMaleNerve Tissue ProteinsRetinaRNA Splicing FactorsAdenosineCyclin-Dependent Kinase 6GlucoseNerve Tissue ProteinsN-methyladenosineRNA Splicing FactorsYTHDC1 protein, humanCDK6m6ARetinal vascular endothelial cellYTHDC1

Identifiers

PMID38978074
PMCPMC11229198

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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.