NLRP3 inflammasome involves in the pathophysiology of sepsis-induced myocardial dysfunction by multiple mechanisms.

Sepsis-induced myocardial dysfunction (SIMD) is one of the serious health-affecting problems worldwide. At present, the mechanisms of SIMD are still not clearly elucidated. The NOD-like receptor protein 3 (NLRP3) inflammasome has been assumed to be involved in the pathophysiology of SIMD by regulating multiple biological processes. NLRP3 inflammasome and its related signaling pathways might affect the regulation of inflammation, autophagy, apoptosis, and pyroptosis in SIMD. A few molecular specific inhibitors of NLRP3 inflammasome (e.g., Melatonin, Ulinastatin, Irisin, Nifuroxazide, and Ginsenoside Rg1, etc.) have been developed, which showed a promising anti-inflammatory effect in a cellular or animal model of SIMD. These experimental findings indicated that NLRP3 inflammasome could be a promising therapeutic target for SIMD treatment. However, the clinical translation of NLRP3 inhibitors for treating SIMD still requires robust in vivo and preclinical trials. [Display omitted] • NLRP3 inflammasome, a pivotal mediator in the activation of the innate immune system in response to infection, has been found to play a key role in the pathophysiology of SIMD. • NLRP3 contributes to the development of SIMD by regulating its targeted genes and signal cascades, which function together on inflammation, autophagy, apoptosis, and pyroptosis. • NLRP3 inflammasome inhibitor exert potential anti-inflammatory effects in SIMD, indicating it may be a potential therapeutic target or preventive agent for SIMD treatment in clinical practice. [ABSTRACT FROM AUTHOR]