Abstract：
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.
摘要：
脓毒症诱发的心肌功能障碍（SIMD）是世界范围内严重影响健康的问题之一。目前,SIMD的机制仍未明确阐明。NOD样受体蛋白3（NLRP3）炎症小体被认为通过调节多个生物学过程参与SIMD的病理生理学。NLRP3炎性体及其相关信号通路可能影响炎症的调节,自噬,凋亡，以及SIMD中的焦亡。NLRP3炎性体的一些分子特异性抑制剂(例如，褪黑激素,乌司他丁,Irisin,硝呋嗪,和人参皂苷Rg1等。)已经开发出来了，在SIMD的细胞或动物模型中显示出有希望的抗炎作用。这些实验结果表明，NLRP3炎性体可能是SIMD治疗的有希望的治疗靶标。然而,用于治疗SIMD的NLRP3抑制剂的临床转化仍需要强有力的体内和临床前试验.
