ArticleEuropace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology2026
Fto-mediated m6A demethylation of Lox drives atrial fibrosis and promotes atrial fibrillation in a murine model of hyperthyroidism.
Article in Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- FTO in cardiovascular diseases: mechanisms, context dependence, and translational opportunities.Frontiers in cell and developmental biology · 2026Review
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Abstract
aimsHyperthyroidism is a risk factor for atrial fibrillation (AF), and N6-methyladenosine (m6A) RNA methylation is crucial in cardiovascular regulation. However, the role of Fto-mediated m6A demethylation in hyperthyroidism-related AF remains unclear. METHODS AND
resultsWe consecutively recruited 232 AF patients undergoing ablation, stratified into age-, gender-, and comorbidity-matched cohorts, 116 with manifest hyperthyroidism and 116 without manifest hyperthyroidism. Assessments included thyroid profiles, echocardiography, low-voltage area (LVA) mapping, and 1-year recurrence. T4-treated mice with cardiomyocyte-specific Fto knockout or AAV9-mediated Fto overexpression were used. Electrophysiological and structural properties were assessed via electrical mapping and echocardiography. Mechanisms were further investigated in neonatal rat atrial myocytes (NRAMs). The hyperthyroid group showed higher 1-year recurrence (19.8 vs. 5.2%, P < 0.001) and larger LVA (27.81 vs. 20.25%, P < 0.001). Hyperthyroidism independently predicted LVA expansion (odds ratio = 2.868, P < 0.001). In mice, Fto up-regulation increased atrial fibrosis and AF susceptibility, while its deletion attenuated T4-induced atrial fibrosis and AF. Wild-type Fto overexpression promoted AF via m6A-dependent enhancement of lysyl oxidase (Lox) expression. Studies in NRAMs demonstrated that Fto enhanced the transcription and translation of Lox by reducing m6A methylation on Lox mRNA. Lox inhibition with BAPN suppressed fibrosis and AF inducibility.
conclusionHyperthyroidism promoted atrial arrhythmogenicity through Fto-mediated m6A demethylation of Lox, increasing Lox expression and atrial fibrosis. Targeting Fto-m6A-Lox may offer a novel therapy for hyperthyroidism-associated AF.
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