Senolytic reduction of senescent cells mitigates atrial arrhythmia vulnerability in aging rabbits.

Elif Sengun, Lily Zhou, Maxfield Kelsey, Nilufer N Turan, Yichun Lu, Anatoli Y Kabakov, Peter Bronk, Eric Mi, Tae Yun Kim, Shilpa Vijayakumar, Dana Price, Sade Solola Nussbaum, Christopher Song, Jun Feng, Frank W Sellke, Patrycja Dubielecka-Szczerba, Federica Del Monte, Jeanne Nerbonne, B Sonmez Uydes-Dogan, Karim Roder, Bum-Rak Choi, David R Van Wagoner, John M Sedivy, Gideon Koren

The Warren Alpert Medical School of Brown University, Providence, Rhode Island; Cardiovascular Research Center, Rhode Island Hospital, Providence, Rhode Island; Department of Pharmacology, Institute of Graduate Studies in Health Sciences, Istanbul University, Istanbul, Türkiye.The Warren Alpert Medical School of Brown University, Providence, Rhode Island; Cardiovascular Research Center, Rhode Island Hospital, Providence, Rhode Island; Department of Pharmacology, Institute of Graduate Studies in Health Sciences, Istanbul University, Istanbul, Türkiye. · pubmed

Paper

Abstract

Atrial 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.

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Research summary

The paper claims that reducing senescent cells can decrease the vulnerability to atrial arrhythmias in aging rabbits. This research is relevant as it addresses cellular senescence, a fundamental aspect of aging, and explores a potential intervention that targets the root causes of age-related diseases.

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