Arrhythmias & electrophysiologyMechanistic study
Fto-mediated m6A demethylation of lysyl oxidase (Lox) drives atrial fibrosis and promotes atrial fibrillation in a murine model of hyperthyroidism
- Mechanistic study
- matched clinical cohorts
- murine model
- cardiomyocyte-specific Fto knockout
- AAV9-mediated Fto overexpression
Authors' conclusion
Hyperthyroidism promoted atrial arrhythmogenicity through Fto-mediated m6A demethylation of Lox, increasing Lox expression and atrial fibrosis.
Study context
- Population
- Atrial fibrillation (AF) patients undergoing ablation; T4-treated mice; neonatal rat atrial myocytes (NRAMs)age-, gender-, comorbidity-matched
- Participants
- 232 patients
- Comparison
- Hyperthyroid vs Without manifest hyperthyroidism
- Hyperthyroidn = 116
- Without manifest hyperthyroidismn = 116reference
Main finding
As reported in the abstract
1-year AF recurrence and LVA (hyperthyroid vs non-hyperthyroid AF patients) · 1 year
Odds ratio
2.868
P < 0.001
Further findings
1-year AF recurrence
P < 0.001
Low-voltage area (LVA)
P < 0.001
| Outcome | OR | P value |
|---|---|---|
| LVA expansion, hyperthyroidism as independent predictor | 2.868 | P < 0.001 |
Original publication
Fto-mediated m6A demethylation of Lox drives atrial fibrosis and promotes atrial fibrillation in a murine model of hyperthyroidism. Europace. Published 11 March 2026. doi:10.1093/europace/euag047
Summarised from the published abstract; every number is checked against it