The senescent heart and atrial fibrillation.
Abstract
Atrial fibrillation (AF) is increasing in prevalence and burden worldwide as the population grays. Aging, a multifaceted universal biological process, is a primary driver of AF development and persistence. However, the mechanistic connection between aging and atrial myopathy, the main substrate for the development and sustenance of AF, remains poorly elucidated. Cellular senescence is a foundational aging component characterized by cell cycle arrest, an antiapoptotic phenotype, and a unique secretome linking it to many chronic and aging-related diseases, including atherosclerosis, arrhythmia, and myocardial diseases. In this review, we discuss the literature on the molecular basis of cardiac senescence and the associated secretory phenotype. Then, we discuss its relationship to atrial myopathy and remodeling through the activation of the renin-angiotensin-aldosterone system, mitochondrial alterations, and epigenetic changes. We then offer insights into preclinical studies on senolytic and senomorphic agents specifically in cardiology and finally discuss the challenges and future directions.
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Research summary
The paper discusses the molecular mechanisms linking cellular senescence to atrial myopathy and atrial fibrillation, suggesting potential therapeutic avenues through senolytic and senomorphic agents. This research is relevant as it addresses the underlying biological processes of aging and their connection to age-related cardiovascular diseases, which is crucial for longevity research.
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