ArticleImmunologic research2025
METTL14 aggravates pyroptosis in diabetic cardiomyopathy by promoting m6A modification of NLRP3.
Article in Immunologic research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The trial behind it
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Who cites it
2 citing papers in PubMed.
- Regulatory mechanisms and therapeutic potential of N6-methyladenosine modification in retinal diseases (Review).Molecular medicine reports · 2026Review
- Integrative multi-omics analysis unveils the regulatory landscape of diabetic cardiomyopathy: from chromatin accessibility to transcript isoforms and epitranscriptome.Frontiers in endocrinology · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
Diabetic cardiomyopathy (DCM) is an irreversible chronic cardiovascular complication of diabetes with a high mortality rate. This study aimed to explore the role of methyltransferase-like 14 (METTL14)-mediated m6A modification in DCM. Here, DCM mouse models and high glucose (HG)-induced H9C2 cell models were employed. Cell phenotype was assessed using CCK-8 assay, lactate dehydrogenase (LDH) assay, Western blot, and flow cytometry. The underlying mechanism was investigated using quantitative real-time PCR (qPCR), methylated RNA immunoprecipitation (MeRIP), RNA immunoprecipitation (RIP), and dual-luciferase reporter assay. The results showed that METTL14 was upregulated in vitro and in vivo. Downregulation of METTL14 inhibited pyroptosis and myocardial damage. Mechanistically, METTL14 enhanced NLRP3 stability through m6A modification of NLRP3. Moreover, the m6A reader protein YTHDF1 (YTH N6-methyladenosine RNA-binding protein 1) mediated NLRP3 upregulation. This study revealed a novel mechanism by which METTL14-mediated m6A methylation regulates DCM progression, providing a potential therapeutic target for DCM.
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Registered trials
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