ArticleHeart rhythm2026
Senolytic reduction of senescent cells mitigates atrial arrhythmia vulnerability in aging rabbits.
Article in Heart rhythm, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Editorial commentary: Targeting senescence to improve cardiac function following myocardial infarction.Trends in cardiovascular medicine · 2026Article
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24 authors.
Funding
Abstract
backgroundAtrial fibrillation (AF) is the most common arrhythmia among the elderly and a major contributor to morbidity and mortality. Inflammation plays a central role in AF pathogenesis, and aging is a key independent risk factor. Cellular senescence is a hallmark of aging and contributes to age-related disease through the senescence-associated secretory phenotype (SASP), characterized by proinflammatory and profibrotic factors.
objectiveThis study aimed to determine whether senescent atrial cells contribute to age-related AF risk and whether senolytic therapy can mitigate this phenotype.
methodsYoung (≤1 year) and aged (≥4 years) New Zealand White rabbits were evaluated using optical mapping, patch-clamp electrophysiology, and histologic and molecular analyses. Senescence markers were assessed using senescence-associated β-galactosidase staining, immunofluorescence, and RNA sequencing. Human atrial specimens from patients with and without AF were examined to assess translational relevance. Aged rabbits received the senolytic compound fisetin to evaluate its effects on atrial senescence and arrhythmia susceptibility.
resultsAged rabbits displayed electrophysiological heterogeneity, prolonged action potentials, and increased AF inducibility, recapitulating clinical features of elderly human atria. Atrial tissue from aged rabbits and patients with AF showed an increase in senescent myocytes and myofibroblasts with upregulation of inflammatory SASP genes. SASP factor expression correlated with left atrial diameter in human samples, an AF risk factor. Short-term fisetin treatment eliminated most senescent atrial cells, reduced inducible AF, and decreased reentry activity without impairing atrial function.
conclusionSenescent 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.
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