Circulation, Ahead of Print. BACKGROUND:Atrial fibrillation (AF) is the most common arrhythmia and is associated with high morbidity and mortality, particularly in the aging population.
Current treatment and prevention strategies remain suboptimal, highlighting the urgent need to better understand the mechanisms underlying aging-associated AF. We recently reported a causal role of the stress-activated kinase JNK2 (c-Jun N-terminal kinase 2) in aging-associated AF pathogenesis, mediated by JNK2-driven sarcoplasmic reticulum Ca2+dysfunction.
However, the mechanisms by which cardiac JNK2 is activated during aging to promote AF remain unclear. Emerging evidence suggests that interorgan crosstalk contributes critically to the development of cardiovascular diseases.
A hyperpermeable gastrointestinal epithelial barrier (“leaky gut”), commonly observed in aged individuals, is associated with elevated levels of proinflammatory cytokines and an increased risk of AF. Although proinflammatory cytokines have been proposed as predisposing factors for AF, clinical and experimental studies have yielded inconsistent results, underscoring the complexity of inflammation-associated AF pathogenesis.
Circulation published a clinical update in Cardiology on 20 Apr 2026.
The item focuses on JNK2 Is a Stress Integrator Driving Atrial Fibrillation Pathogenesis in Aging via Gut-Heart Crosstalk.
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