Key result
Aging drives AF risk via mechanisms including fibrosis, DNA damage, and mitochondrial dysfunction.
Why the study?
Aging is a major risk factor for atrial fibrillation, but the specific biological and pathophysiological mechanisms underlying this association remain poorly understood.
This review highlights the pathophysiological mechanisms driving the association between aging and atrial fibrillation, emphasizing areas for future research.
Aging is one of the most significant risk factors for the development of atrial fibrillation, and given our aging population, this is likely to present a major public health challenge in the coming years. Although the specific mechanisms underlying this association remain poorly understood, several biological processes including fibrosis, DNA damage, chromatin remodeling, amyloid deposition, mitochondrial dysfunction, and inflammation have been implicated in the structural and functional deterioration that leads to the development of atrial fibrillation. Herein, we review work from the last several years that has contributed to our understanding of the link between aging and atrial fibrillation with a focus on the basic pathophysiological mechanisms. We also outline areas for future research aimed at better characterizing this complex relationship.
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Ryan et al. (2025) conducted a review in Atrial fibrillation. Aging was evaluated. Aging is a major risk factor for atrial fibrillation, driven by pathophysiological mechanisms including fibrosis, DNA damage, chromatin remodeling, amyloid deposition, and mitochondrial dysfunction.
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