ReviewMolecular therapy : the journal of the American Society of Gene Therapy2024
m6A epitranscriptomic and epigenetic crosstalk in cardiac fibrosis.
Review in Molecular therapy : the journal of the American Society of Gene Therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- RNA methylation in cardiovascular remodeling: Molecular mechanisms, biomarkers, and therapeutic strategies.Molecular biology reports · 2026Review
- m6A-Mediated epitranscriptional reprogramming drives cardiac fibrosis by suppressing PGC-1α and boosting mitochondrial fission.Journal of translational medicine · 2026Article
- MicroRNAs in Heart Failure Pathogenesis and Progression: Mechanistic Control, Biomarker Potential, and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
- Therapy-induced mRNA, rRNA and tRNA methylation alterations confer tolerance phenotype in tumor cells: mechanism and implications.International journal of biological sciences · 2026Review
- The translational potential of m6A RNA methylation in DKD: emerging biomarkers for early detection and targeted therapies.Frontiers in medicine · 2026Review
- Epitranscriptomic regulation of endothelial plasticity under hemodynamic forces: insights from the KLF2/4-METTL3-H19 pathway.Frontiers in genetics · 2026Review
- ALKBH5-mediated RNA N6-methyladenosine demethylation protects against myocardial I/R-induced injury via FSP1-dependent inhibition of ferroptosis.Journal of molecular histology · 2025Article
- Epitranscriptomic modifications in programmed cell death: mechanistic insights and implications for liver diseases.Cellular & molecular biology letters · 2025Review
- RNA Modifications in Health and Disease.MedComm · 2025Review
- Dynamic modifications of circular RNAs drive oncogenesis.Epigenomics · 2025Review
- ALKBH5 regulates intrauterine adhesion progression through m6A dependent FABP4 mRNA stabilization and serum lipid metabolism.Communications biology · 2025Article
- METTL3 promotes the hypertrophic scar fibrosis via m6A RNA methylation of GRAMD1B mRNA.Journal of molecular histology · 2025Article
- RNA and epigenetic editing: The new frontier in gene and cell therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The epigenetic regulation of crosstalk between cardiac fibroblasts and other cardiac cell types during stress.Frontiers in cardiovascular medicine · 2025Review
- Deciphering single-cell landscape unravels cell-type-specific functional roles of RNA mTheranostics · 2025Article
- NCardiovascular diabetology · 2024Article
- Role of M6a Methylation in Myocardial Ischemia-Reperfusion Injury and Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2024Review
- ALKBH5-mediated mClinical and translational medicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis, a crucial pathological characteristic of various cardiac diseases, presents a significant treatment challenge. It involves the deposition of the extracellular matrix (ECM) and is influenced by genetic and epigenetic factors. Prior investigations have predominantly centered on delineating the substantial influence of epigenetic and epitranscriptomic mechanisms in driving the progression of fibrosis. Recent studies have illuminated additional avenues for modulating the progression of fibrosis, offering potential solutions to the challenging issues surrounding fibrosis treatment. In the context of cardiac fibrosis, an intricate interplay exists between m6A epitranscriptomic and epigenetics. This interplay governs various pathophysiological processes: mitochondrial dysfunction, mitochondrial fission, oxidative stress, autophagy, apoptosis, pyroptosis, ferroptosis, cell fate switching, and cell differentiation, all of which affect the advancement of cardiac fibrosis. In this comprehensive review, we meticulously analyze pertinent studies, emphasizing the interplay between m6A epitranscriptomics and partial epigenetics (including histone modifications and noncoding RNA), aiming to provide novel insights for cardiac fibrosis treatment.
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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.