ArticleCardiovascular drugs and therapy2023
Mechanism of METTL3-Mediated m
Article in Cardiovascular drugs and therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
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.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- METTL3 Confers Ischemia/Reperfusion-Caused Myocardial Injury by Triggering Ferroptosis via Regulating the lncRNA SNHG14/miR-195a-5p/ACSL4 Axis.Cardiovascular drugs and therapy · 2026Article
- The mechanism of m6A modification in cardiovascular diseases: A systematic review.Genes & diseases · 2026Review
- Pyroptosis Regulated by N6-Methyladenosine Modification: Implications for Pyroptosis-Related Disease Therapy.Journal of innate immunity · 2026Review
- m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling.European journal of medical research · 2025Review
- Mitochondria at the intersections of RNA modifications and metabolism reprogramming implications in cell death, tumor microenvironment, and immunotherapy.Journal of hematology & oncology · 2025Review
- METTL3 mediates CPB1 expression by regulating transcription factor BACH2 to promote apoptosis and oxidative stress of lens epithelial cells.Journal of bioenergetics and biomembranes · 2025Article
- METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential.Cell biology and toxicology · 2025Review
- Review
- m6A Ribonucleic Acid Methylation in Fibrotic Diseases of Visceral Organs.Small science · 2025Review
- Novel Insight of N6-Methyladenosine in Cardiovascular System.Medicina (Kaunas, Lithuania) · 2025Review
- Emerging mechanisms and implications of m6A in CVDs: potential applications of natural products.Frontiers in cardiovascular medicine · 2025Review
- The N-6 methyladenosine dynamics in STEMI and the effect of IL-6 inhibition - a hypothesis generating sub-study of the ASSAIL-MI trial.Frontiers in immunology · 2025Article
- Aerobic exercise inhibits GSDME-dependent myocardial cell pyroptosis to protect ischemia-reperfusion injury.Molecular medicine (Cambridge, Mass.) · 2024Article
- METTL3, m6A modification, and EGR1: interplay affecting myocardial I/R injury outcomes.Cell biology and toxicology · 2024Article
- MGenes & diseases · 2024Review
- Specific deletion of Mettl3 in IECs triggers the development of spontaneous colitis and dysbiosis of T lymphocytes in mice.Clinical and experimental immunology · 2024Article
- METTL14-mediated N6-methyladenosine modification induces the ferroptosis of hypoxia/reoxygenation-induced cardiomyocytes.Journal of cardiothoracic surgery · 2024Article
- Novel Insights into the Links between N6-Methyladenosine and Regulated Cell Death in Musculoskeletal Diseases.Biomolecules · 2024Review
- Mesenchymal Stem Cells-Derived Exosomes Alleviate Acute Lung Injury by Inhibiting Alveolar Macrophage Pyroptosis.Stem cells translational medicine · 2024Article
- m6A epitranscriptomic and epigenetic crosstalk in cardiac fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveMyocardial ischemia/reperfusion (MI/R) injury is a complicated pathophysiological process associated with cardiomyocyte pyroptosis. Methyltransferase-like protein 3 (METTL3) catalyzes the formation of N
methodsA rat model of MI/R was established. Rat cardiomyocytes were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) treatment for the establishment of a cell model in vitro. METTL3 expression in myocardial tissues of MI/R rats and OGD/R-treated cardiomyocytes was determined using RT-qPCR and Western blot. The pathological changes of rat myocardial tissues were observed using hematoxylin and eosin staining. The positive expression of NLRP3 in myocardial tissues or cardiomyocytes was observed through immunohistochemistry or immunofluorescence. The activity of caspase-1 was measured using the colorimetric method. The expressions of GSDMD and cleaved caspase-1, as well as the levels of IL-1β and IL-18 in rat myocardial tissues or cardiomyocytes were determined. m
resultsMETTL3 expression was elevated in MI/R rats and OGD/R cardiomyocytes. METTL3 silencing alleviated myocardial injury, reduced the number of NLRP3-positive cardiomyocytes, suppressed caspase-1 activity, decreased the protein levels of GSDMD-N and cleaved caspase-1, and decreased IL-1β and IL-18 levels. METTL3 increased the total m
conclusionMETTL3 promoted DGCR8 binding to pri-miR-143-3p through m
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Registered trials
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.