Evidence map›Paper›PMID 34825733›Full record

ArticleJournal of clinical laboratory analysis2022

Mettl3 promotes oxLDL-mediated inflammation through activating STAT1 signaling.

Zhenwei Li, Qingqing Xu, Ning Huangfu, Xiaomin Chen, Jianhua Zhu

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 5% of its field
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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. METTL3-mCellular & molecular biology letters · 2026
    Article
  3. mFrontiers in immunology · 2026
    Review
  4. Article
  5. Review
  6. METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025
    Review
  7. A comprehensive review of m6 A methylation in coronary heart disease.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  8. Review
  9. Review
  10. The role of mFrontiers in immunology · 2025
    Review
  11. Article
  12. NAging and disease · 2024
    Review
  13. Review
  14. Insights into the role of RNA mGenes & diseases · 2024
    Review
  15. Transcriptome-wide NBMC genomics · 2023
    Article
  16. Article
  17. Review
  18. Review
  19. The Mechanism and Role ofJournal of cardiovascular development and disease · 2022
    Review
  20. 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

5 authors at 3 institutions in 1 country.

Zhenwei LiDepartment of Cardiology, The first Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Qingqing XuDepartment of Nephrology, Ningbo First Hospital, Ningbo, China.
Ning HuangfuDepartment of Cardiology, Ningbo Hospital of Zhejiang University, Ningbo, China.
Xiaomin ChenDepartment of Cardiology, Ningbo Hospital of Zhejiang University, Ningbo, China.ORCID https://orcid.org/0000-0003-1498-0452
Jianhua ZhuDepartment of Cardiology, The first Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
First Affiliated Hospital Zhejiang University · CNZhejiang University · CNNingbo First Hospital · CN

Funding

Ningbo Health Branding Subject Fund PPXK2018-01Zhejiang Provincial Natural Science Foundation of China LY19H020003Zhejiang Provincial Natural Science Foundation of China LY19H310002
6 · The paper itself

Abstract

backgroundAtherosclerosis (AS) is the main cause of cerebrovascular diseases, and macrophages act important roles during the AS pathological process through regulating inflammation. Modification of the novel N(6)-methyladenine (m6A) RNA is reported to be associated with AS, but its role in AS is largely unknown. The aim of this study was to investigate the role and mechanism of m6A modification in inflammation triggered by oxidized low-density lipoprotein (oxLDL) in macrophages during AS.

methodsRAW264.7 macrophage cells were stimulated with 40 μg/ml ox-LDL, Dot blot, Immunoprecipitation, western blot, Rip and chip experiments were used in our study.

resultsWe found oxLDL stimulation significantly promoted m6A modification level of mRNA in macrophages and knockdown of Methyltransferase-Like Protein 3 (Mettl3) inhibited oxLDL-induced m6A modification and inflammatory response. Mettl3 promoted oxLDL-induced inflammatory response in macrophages through regulating m6A modification of Signal transducer and activator of transcription 1 (STAT1) mRNA, thereby affecting STAT1 expression and activation. Moreover, oxLDL stimulation enhanced the interaction between Mettl3 and STAT1 protein, promoting STAT1 transcriptional regulation of inflammatory factor expression in macrophages eventually.

conclusionsThese results indicate that Mettl3 promotes oxLDL-triggered inflammation through interacting with STAT1 protein and mRNA in RAW264.7 macrophages, suggesting that Mettl3 may be as a potential target for the clinical treatment of AS.

Indexed as

AdenineAnimalsAtherosclerosisHumansInflammationLipoproteins, LDLMacrophagesMethyltransferasesMiceRAW 264.7 CellsRNA, MessengerSignal TransductionSTAT1 Transcription Factor6-methyladenineAdenineLipoproteins, LDLMethyltransferasesMettl3 protein, mouseoxidized low density lipoproteinRNA, MessengerStat1 protein, mouseSTAT1 Transcription Factoratherosclerosisinflammationmethyltransferase-like protein 3N6-methyladenosinesignal transducer and activator of transcription 1

Identifiers

PMID34825733
PMCPMC8761454
OpenAlexW3152872378

What OpenQuestion holds

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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.