Senescent cells drive prolonged cardiac damage after heart attack

Senescent cells—those that arrest division following injury—carry a paradoxical role in cardiac recovery: initially they coordinate tissue repair, yet when they persist beyond healing, particularly after myocardial infarction, they trigger a chronic inflammatory cascade that compounds damage. The core mechanism is the SASP (senescence-associated secretory phenotype), a secretory profile that unfolds across three distinct phases: acute inflammation amplification in the first days, then inflammation resolution and scar formation, before pivoting to chronic fibrosis and ventricular dysfunction. This spatiotemporal reconfiguration of SASP simultaneously influences the infarct zone, the border transitional region, and compensatory areas of the heart. For researchers, the therapeutic window is precise: senolytic intervention—selective destruction of these cells—applied at the exact moment could interrupt the dysfunctional cascade before chronic insufficiency solidifies, positioning this approach as a major frontier in cardiac regenerative medicine.