Abstract
Sepsis is a systemic inflammatory response syndrome triggered by infection, in which excessive immune responses can lead to multiple organ failure and shock. The heart, as one of the critical target organs in sepsis, is significantly impaired, which substantially increases the risk of mortality. Recent studies have increasingly highlighted the role of dysregulated inflammatory responses in the pathogenesis and progression of sepsis-induced myocardial dysfunction (SIMD). Among the key molecular mechanisms regulating various pathophysiological processes and modulating inflammation is the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3(NLRP3) inflammasome. This study aims to explore the role of the NLRP3 inflammasome in the pathogenesis of SIMD, with a focus on its involvement through pathways such as pyroptosis, oxidative stress, autophagy, mitochondrial damage, exosome release, and endoplasmic reticulum stress in the development of SIMD. Furthermore, the research seeks to uncover the potential key roles of the NLRP3 inflammasome in the underlying pathophysiological mechanisms of SIMD. Finally, the study will investigate NLRP3 inflammasome-based therapeutic strategies for targeting SIMD, providing theoretical support for the development of targeted management for SIMD.