Epigenetics in Atrial Fibrillation: Molecular Mechanisms and Therapeutic Avenues.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic literature without systematic search or meta-analysis
PubMed 42534251 · doi:10.31083/RCM49551
What was done
This narrative review summarizes current literature on the roles of multiple epigenetic mechanisms—including DNA methylation, histone modifications, non-coding RNAs (miRNAs, lncRNAs, circRNAs, and tsRNAs), chromatin remodeling, and RNA methylation—in the pathogenesis of atrial fibrillation (AF). It specifically examines how these pathways influence atrial structural and electrical remodeling, their utility as circulating biomarkers, and potential epigenetic-targeted pharmacotherapies.
What was found
The abstract reports no quantitative results, effect sizes, or study counts. It qualitatively reports that reversible epigenetic modifications regulate critical gene expression underlying AF remodeling, highlights circulating epigenetic markers (such as methylated DNA and miRNAs) for risk stratification and relapse prediction, and identifies epigenetic modulators (such as histone deacetylase inhibitors and demethylating agents) as potential therapeutic avenues.
Why it matters
The paper consolidates molecular mechanisms linking epigenetic alterations to atrial remodeling, framing potential directions for precision diagnosis, risk prediction, and novel drug development in atrial fibrillation.
Limits
The abstract reports no original human or animal data and no quantitative meta-analysis. It does not provide specific sample sizes, search parameters, or study selection criteria, limiting the assessment of bias in the summarized literature. Furthermore, the clinical safety and efficacy of proposed epigenetic interventions remain unestablished in this text.
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- supports Atrial fibrillation is the most common cardiac dysrhythmia.