![]() Our findings suggest that therapeutic interventions targeting senescent cells may mitigate arrhythmias post-MI with age. ![]() Aged infarcted human ventricles show levels of senescence consistent with aged rabbits, and senescent myofibroblasts also couple to IBZ myocytes. Senescent IBZ myofibroblasts in aged rabbits appear to be coupled to myocytes, and our computational modeling showed that senescent myofibroblast-cardiomyocyte coupling prolongs action potential duration (APD) and facilitates conduction block permissive of arrhythmias. Studies of the aged infarct zone revealed persistent myofibroblast senescence and increased inflammatory signaling over a 12-week timecourse. Aged rabbits exhibited increased peri-procedural mortality and arrhythmogenic electrophysiological remodeling at the infarct border zone (IBZ) compared to young rabbits. Here, we investigated the role of senescence in regulating inflammation, fibrosis, and arrhythmogenesis in young and aged infarcted rabbits. Additionally, the cellular and systemic role of senescence and its inflammatory milieu in influencing arrhythmogenesis with age is not clear, particularly in large animal models with cardiac electrophysiology more similar to humans than previously studied animal models. Specifically, age-associated changes in timecourse of senescence and related changes in inflammation and fibrosis are not well understood. Senescent cells interfere with cardiac function and outcome post-MI with age, but studies have not been performed in larger animals, and the mechanisms are unknown. Senescent cells accumulate with age and accelerate age-associated diseases. ![]() ![]() This process is well studied in young animals, but little is known about pro-arrhythmic changes in aged animals. Progressive tissue remodeling after myocardial infarction (MI) promotes cardiac arrhythmias. ![]()
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