ReviewCells2022
Emerging Roles and Mechanism of m6A Methylation in Cardiometabolic Diseases.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed.
- PDE4D Mediates the Cardiac Ischemia Reperfusion Injury and Is m6A Modified by METTL14.Korean circulation journal · 2026Article
- METTL14 Promotes Cuproptosis-Associated Changes in Rats With Myocardial Ischemia-Reperfusion Injury.Journal of cellular biochemistry · 2026Article
- The mechanism of m6A modification in cardiovascular diseases: A systematic review.Genes & diseases · 2026Review
- The spatiotemporal dynamic evolution of post-stroke neuroinflammation: energy metabolism mechanisms of acute response and chronic progression.Frontiers in pharmacology · 2026Review
- mFrontiers in immunology · 2026Review
- m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling.European journal of medical research · 2025Review
- METTL3/RBM15 augments the stability of Kdm6b mRNA and promotes STAT1-mediated macrophage activation and atherosclerosis.Experimental & molecular medicine · 2025Article
- Advances in RNA modification in myocardial fibrosis (Review).International journal of molecular medicine · 2025Review
- METTL14-mediated mEpigenetics · 2025Article
- M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury.Redox report : communications in free radical research · 2025Article
- Associations of circadian syndrome with gout and hyperuricemia: a cross‑sectional analysis of NHANES 2007-2018.BMC public health · 2025Article
- Transcriptome-wide N6-methyladenosine methylation dynamic profile in type 1 diabetes progression.Epigenomics · 2025Article
- WTAP-mediated N6-methyladenine Modification of circEEF2 Promotes Lung Adenocarcinoma Tumorigenesis by Stabilizing CANT1 in an IGF2BP2-dependent Manner.Molecular biotechnology · 2025Article
- Molecular mechanisms of m6A modifications regulating tumor radioresistance.Molecular medicine (Cambridge, Mass.) · 2025Review
- [Research progress on N6-methyladenosine and ferroptosis in childhood combined allergic rhinitis and asthma syndrome].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Review
- ALKBH5 alleviates lower extremity arteriosclerosis by regulating ITGB1 demethylation and influencing macrophage polarization.Heliyon · 2025Article
- Macrophage-driven immunopathology in pulmonary arterial hypertension: from mechanisms to targeted therapies.Frontiers in immunology · 2025Review
- Landscape analysis of m6A modification regulators reveals LRPPRC as a key modulator in tubule cells for DKD: a multi-omics study.Frontiers in pharmacology · 2025Article
- Insights From m6A RNA Methylation: Biomarkers for Diagnosis of Acute Myocardial Infarction.Journal of inflammation research · 2025Article
- Deciphering single-cell landscape unravels cell-type-specific functional roles of RNA mTheranostics · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiometabolic diseases (CMDs) are currently the leading cause of death and disability worldwide, and their underlying regulatory mechanisms remain largely unknown. N6-methyladenosine (m6A) methylation, the most common and abundant epigenetic modification of eukaryotic mRNA, is regulated by m6A methyltransferase, demethylase, and the m6A binding protein, which affect the transcription, cleavage, translation, and degradation of target mRNA. m6A methylation plays a vital role in the physiological and pathological processes of CMDs. In this review, we summarize the role played by m6A methylation in CMDs, including obesity, hypertension, pulmonary hypertension, ischemic heart disease, myocardial hypertrophy, heart failure, and atherosclerosis. We also describe mechanisms that potentially involve the participation of m6A methylation, such as those driving calcium homeostasis, circadian rhythm, lipid metabolism, autophagy, macrophage response, and inflammation. m6A methylation and its regulators are expected to be targets for the treatment of CMDs.
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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.