ArticleCirculation2019
The N
Article in Circulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04533282 (Epitranscriptomic Biomarkers for Ischemic Heart Disease), which is not on this map. Cited by 312 papers.
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.
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.
Epitranscriptomic Biomarkers for Ischemic Heart Disease (IHD-EPITRAN) - A Prospective Cohort Study
Who cites it
312 citing papers in PubMed, 456 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
- m6A methylation in ferroptosis regulation: mechanisms, targets, and therapeutic interventions.Journal of advanced research · 2026Review
- METTL14-Mediated mAging cell · 2026Article
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
- METTL14-Mediated N6-Methyladenosine Exacerbates Acute Lung Injury via USP30/NCOA4-Dependent Ferroptosis.MedComm · 2026Article
- Article
- METTL14 Promotes Cuproptosis-Associated Changes in Rats With Myocardial Ischemia-Reperfusion Injury.Journal of cellular biochemistry · 2026Article
- Trdn-as directs m6A-dependent transcriptional termination for accurate triadin isoform switching, preventing aberrant dyads and cardiomyopathy.Nature communications · 2026Article
- PYRIN mActa pharmacologica Sinica · 2026Article
- Review
- KuJiang GanLuoYin Alleviates Hypertensive Vascular Injury and Modulates FMO2/FTO/mBiomedicines · 2026Article
- mRedox biology · 2026Review
- The Role of NMedComm · 2026Review
- RNA methylation in cardiovascular remodeling: Molecular mechanisms, biomarkers, and therapeutic strategies.Molecular biology reports · 2026Review
- METTL3 mediates mJournal of advanced research · 2026Article
- METTL3-mediated mJournal of translational medicine · 2026Article
- m6A-Mediated epitranscriptional reprogramming drives cardiac fibrosis by suppressing PGC-1α and boosting mitochondrial fission.Journal of translational medicine · 2026Article
- Dynamic m⁶A methylation during bovine preadipocyte differentiation and functional implication of the m⁶A writer METTL14.BMC genomics · 2026Article
- METTL14-dependent mbioRxiv : the preprint server for biology · 2026Article
- METTL3-mediated N6-methyladenosine modification ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
252 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
backgroundN
methodsTo determine the role of m6A methylation in the heart, we isolated primary cardiomyocytes and performed m6A immunoprecipitation followed by RNA sequencing. We then generated genetic tools to modulate m6A levels in cardiomyocytes by manipulating the levels of the m6A RNA methylase methyltransferase-like 3 (METTL3) both in culture and in vivo. We generated cardiac-restricted gain- and loss-of-function mouse models to allow assessment of the METTL3-m6A pathway in cardiac homeostasis and function.
resultsWe measured the level of m6A methylation on cardiomyocyte mRNA, and found a significant increase in response to hypertrophic stimulation, suggesting a potential role for m6A methylation in the development of cardiomyocyte hypertrophy. Analysis of m6A methylation showed significant enrichment in genes that regulate kinases and intracellular signaling pathways. Inhibition of METTL3 completely abrogated the ability of cardiomyocytes to undergo hypertrophy when stimulated to grow, whereas increased expression of the m6A RNA methylase METTL3 was sufficient to promote cardiomyocyte hypertrophy both in vitro and in vivo. Finally, cardiac-specific METTL3 knockout mice exhibit morphological and functional signs of heart failure with aging and stress, showing the necessity of RNA methylation for the maintenance of cardiac homeostasis.
conclusionsOur study identified METTL3-mediated methylation of mRNA on N
Indexed as
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What OpenQuestion holds
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.