Cardiomyocyte death in sepsis: Mechanisms and regulation

Sepsis-induced cardiac dysfunction is one of the most common types of organ dysfunction in sepsis; its pathogenesis is highly complex and not yet fully understood. Cardiomyocytes serve a key role in the pathophysiology of cardiac function; due to the limited ability of cardiomyocytes to regenerate, their loss contributes to decreased cardiac function. The activation of inflammatory signalling pathways affects cardiomyocyte function and modes of cardiomyocyte death in sepsis. Prevention of cardiomyocyte death is an important therapeutic strategy for sepsis-induced cardiac dysfunction. Thus, understanding the signalling pathways that activate cardiomyocyte death and cross-regulation between death modes are key to finding therapeutic targets. The present review focused on advances in understanding of sepsis-induced cardiomyocyte death pathways, including apoptosis, necroptosis, mitochondria-mediated necrosis, pyroptosis, ferroptosis and autophagy. The present review summarizes the effect of inflammatory activation on cardiomyocyte death mechanisms, the diversity of regulatory mechanisms and cross-regulation between death modes and the effect on cardiac function in sepsis to provide a theoretical basis for treatment of sepsis-induced cardiac dysfunction.