ReviewFrontiers in genetics2022
m6A Methylation in Cardiovascular Diseases: From Mechanisms to Therapeutic Potential.
Review in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
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Who cites it
35 citing papers in PubMed, 43 citations in OpenAlex.
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
- METTL3 Promotes Lipid Deposition and Pulmonary Fibrosis by Destabilizing PLIN2 in a m6A-Dependent Manner.Journal of cellular and molecular medicine · 2026Article
- Beyond the Pump: Unravelling Immunometabolic Crosstalk and Organelle Dynamics in Sepsis-Induced Cardiomyopathy.Journal of cardiovascular translational research · 2026Article
- N6-methyladenosine (m6A) post-transcriptional modification regulation of mRNA, an overlooked therapeutic opportunity to leverage mRNA processing in vascular smooth muscle cells.Vascular pharmacology · 2026Review
- Genetic Evidence Supports a Potential Role of WTAP-related m6A Regulation in Vascular Dementia: Insights from Mendelian Randomization and Multi-omics Analyses.Journal of molecular neuroscience : MN · 2026Article
- Pyroptosis Regulated by N6-Methyladenosine Modification: Implications for Pyroptosis-Related Disease Therapy.Journal of innate immunity · 2026Review
- Integrative multi-omics analysis unveils the regulatory landscape of diabetic cardiomyopathy: from chromatin accessibility to transcript isoforms and epitranscriptome.Frontiers in endocrinology · 2026Article
- N6-methyladenosine as a potential epitranscriptomic immune rheostat during SARS-CoV-2 infection.Frontiers in immunology · 2026Review
- Deregulation of m6A-RNA methylation impairs adaptive hypertrophic response and drives maladaptation via mTORC1-S6K1-hyperactivation and autophagy impairment.Cell communication and signaling : CCS · 2025Article
- Epigenetic modifier m⁶A methylation: insights into the pathogenesis and therapeutic potential of autoimmune diseases.Journal of translational medicine · 2025Review
- PARP1 contributes to intimal hyperplasia by regulating METTL3-mediated m6A methylation of TRAIL.Cell biology and toxicology · 2025Article
- mExperimental & molecular medicine · 2025Review
- Crosstalk between N6-methyladenosine modification and ncRNAs in rheumatic diseases: therapeutic and diagnostic implications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- WTAP Promotes Atherosclerosis by Inducing Macrophage Pyroptosis and M1 Polarization through Upregulating NLRP3.Applied biochemistry and biotechnology · 2025Article
- M6A-modified BFSP1 induces aerobic glycolysis to promote liver cancer growth and metastasis through upregulating tropomodulin 4.Molecular biomedicine · 2025Article
- Identifying common pathways for doxorubicin and carfilzomib-induced cardiotoxicities: transcriptomic and epigenetic profiling.Scientific reports · 2025Article
- Dapagliflozin Suppresses High Glucose-Induced Proliferation, Oxidative Stress, and Fibrosis by Reducing Mettl3-Induced m6A Modification in Marcks mRNA.Cardiovascular toxicology · 2025Article
- Multi-omics approach to personalised treatment: insights into thrombus-derived exosome regulation in cardiomyocyte ferritinophagy.Frontiers in immunology · 2025Article
- WTAP-mediated mRedox report : communications in free radical research · 2024Article
- Non-coding RNAs as therapeutic targets and biomarkers in ischaemic heart disease.Nature reviews. Cardiology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. Recent studies have shown that n6-methyladenosine (m6A) plays a major role in cardiovascular homeostasis and pathophysiology. These studies have confirmed that m6A methylation affects the pathophysiology of cardiovascular diseases by regulating cellular processes such as differentiation, proliferation, inflammation, autophagy, and apoptosis. Moreover, plenty of research has confirmed that m6A modification can delay the progression of CVD via the post-transcriptional regulation of RNA. However, there are few available summaries of m6A modification regarding CVD. In this review, we highlight advances in CVD-specific research concerning m6A modification, summarize the mechanisms underlying the involvement of m6A modification during the development of CVD, and discuss the potential of m6A modification as a therapeutic target of CVD.
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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.