Aging-associated atrial fibrillation: A comprehensive review focusing on the potential mechanisms

Atrial fibrillation (AF) has been receiving a lot of attention from scientists and clinicians because it is an extremely common clinical condition. Due to its special hemodynamic changes, AF has a high rate of disability and mortality. So far, although AF has some therapeutic means, it is still an incurable disease because of its complex risk factors and pathophysiologic mechanisms, which is a difficult problem for global public health. Age is an important independent risk factor for AF, and the incidence of AF increases with age. To date, there is no comprehensive review on aging-associated AF. In this review, we systematically discuss the pathophysiologic evidence for aging-associated AF, and in particular explore the pathophysiologic mechanisms of mitochondrial dysfunction, telomere attrition, cellular senescence, disabled macroautophagy, and gut dysbiosis involved in recent studies with aging-associated AF. We hope that by exploring the various dimensions of aging-associated AF, we can better understand the specific relationship between age and AF, which may be crucial for innovative treatments of aging-associated AF. Our review highlights the potential mechanisms of aging-associated atrial fibrillation, and in particular describes the potential relationship between new aging features and aging-associated atrial fibrillation, including mitochondrial dysfunction, telomere attrition, cellular senescence, macroautophagy dysfunction, and gut dysbiosis, to deepen our understanding of the mechanisms of aging-associated atrial fibrillation and to contribute to the individualized therapeutic strategies for elderly patients with atrial fibrillation.image