The Role of Pyroptosis in Exacerbating Sepsis-Induced Myocardial Injury: Mechanisms and Implications

Sepsis is a life-threatening condition with high morbidity and mortality, wherein sepsis-induced myocardial injury (SIMI) represents a primary cause of acute cardiac insufficiency and adverse outcomes. Pyroptosis, a form of programmed cell death (PCD) mediated by inflammasomes, is capable of sensing cytoplasmic contamination or perturbation. With the continuous advancement of research, growing evidence indicates that pyroptosis serves as a key participant in the pathophysiological basis of SIMI. When the body senses pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), the inflammasome is activated not only in various cardiomyocytes (CMs) but also in non-cardiomyocytes (non-CMs) such as cardiac fibroblasts (CFs), endothelial cells (ECs) and macrophages. Pyroptosis in CMs directly compromises contractile function and causes irreversible cell loss, whereas in non-CMs it predominantly triggers an inflammatory storm and promotes fibrotic and vascular remodeling, thereby indirectly amplifying myocardial injury. This review systematically elaborates on the molecular mechanisms and roles of pyroptosis in SIMI, discusses its potential translational prospects as a therapeutic strategy, and provides a theoretical basis for developing intervention strategies targeting pyroptosis to improve patient prognosis.