Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies  (Review)

Sepsis is a systemic inflammatory disorder characterized by multi-organ dysfunction following infection.Sepsis-induced cardiomyopathy (SIC) represents a prevalent complication that markedly contributes to in-hospital mortality.The NOD-like receptor protein 3 (NLRP3) inflammasome serves as an important regulator in SIC pathogenesis, directly impairing cardiac function through multiple mechanisms: i) Driving cytokine storms; ii) inducing cardiomyocyte pyroptosis and apoptosis; iii) disrupting mitochondrial homeostasis; and iv) suppressing autophagy.Molecularly-targeted NLRP3 inhibitors have been developed, such as MCC950, curcumin, indole-3-propionic acid and carvacrol, which have demonstrated cardioprotective effects in cellular and animal models of SIC.Further exploration of NLRP3 mechanisms and resulting therapeutic targets may yield novel strategies for SIC diagnosis and clinical management.The present review examined NLRP3-mediated pathways involving inflammation, programmed cell death and mitophagy in SIC pathogenesis, summarized pharmacological interventions targeting these pathways and highlighted previous advances in NLRP3 research to inform future therapeutic development and clinical translation.Contents 1. Introduction 2. Biological characteristics of the NLRP3 inflammasome 3. Core mechanisms of NLRP3 inflammasome-driven SIC pathogenesis 4. Interplay of molecular mechanisms 5. Clinical translation challenges and future directions 6. Conclusions