Arrhythmias & electrophysiologyMechanistic study
Senolytic reduction of senescent cells mitigates atrial arrhythmia vulnerability in aging rabbits
- Experimental animal study with human atrial specimens
Authors' conclusion
Senescent atrial cells promote a proinflammatory, proarrhythmic substrate predisposing to AF. Senolytic therapy with fisetin alleviates this phenotype, suggesting a potential strategy to prevent age-related AF.
Study context
- Population
- Young and aged New Zealand White rabbits; human atrial specimens from patients with and without atrial fibrillation (AF)
- Comparison
- Aged vs young rabbits; fisetin treatment in aged rabbits
Main finding
As reported in the abstract
Atrial electrophysiology in aged rabbits
- Aged rabbits displayed electrophysiological heterogeneity, prolonged action potentials, and increased AF inducibility
Further findings
Senescent atrial cells
- Atrial tissue from aged rabbits and patients with AF showed an increase in senescent myocytes and myofibroblasts with upregulation of inflammatory senescence-associated secretory phenotype (SASP) genes
SASP factor expression and left atrial diameter (human)
- SASP factor expression correlated with left atrial diameter in human samples
Effect of short-term fisetin
- Eliminated most senescent atrial cells, reduced inducible AF, and decreased reentry activity without impairing atrial function
Original publication
Senolytic reduction of senescent cells mitigates atrial arrhythmia vulnerability in aging rabbits. Heart Rhythm. Published 7 January 2026. doi:10.1016/j.hrthm.2026.01.007
Summarised from the published abstract; every number is checked against it