NLRP3 inflammasome activation in macrophages fuels sterile inflammation, which has been tied with metabolic reprogramming characterized by high glycolysis and low oxidative phosphorylation. The key enzymes in glycolysis and glycolysis‐related products can regulate and activate NLRP3 inflammasome. In turn, NLRP3 inflammasome is considered to affect glycolysis, as well. However, the exact mechanism remains ambiguous. On the basis of these findings, the focus of this review is mainly on the developments in our understanding of interaction between NLRP3 inflammasome activation and glycolysis in macrophages, and small molecule compounds that influence the activation of NLRP3 inflammasomes by regulating glycolysis in macrophages. The application of this interaction in the treatment of diseases is also discussed. This paper may yield valuable clues for development of novel therapeutic agent for NLRP3 inflammasome‐related diseases.

Chronic low-grade inflammation has been identified as a major contributor in the development of atherosclerosis. Nuclear Factor-κappa B (NF-κB) is a critical transcription factors family of the inflammatory pathway. As a major catalytic subunit of the IKK complex, IκB kinase β (IKKβ) drives canonical activation of NF-κB and is implicated in the link between inflammation and atherosclerosis, making it a promising therapeutic target. Various natural product derivatives, extracts, and synthetic, show anti-atherogenic potential by inhibiting IKKβ-mediated inflammation. This review focuses on the latest knowledge and current research landscape surrounding anti-atherosclerotic drugs that inhibit IKKβ. There will be more opportunities to fully understand the complex functions of IKKβ in atherogenesis and develop new effective therapies in the future.

Heart failure (HF) is a leading cause of mortality worldwide. The pathogenesis of HF is complex and has not yet been fully elucidated, which has slowed drug development and long-term treatments. Inflammasome-mediated responses occur during the progression of HF. It has been reported that energy metabolism and metabolites of intestinal flora are also involved in the process of HF, and they interact with each other to promote the progression of HF. NLR family pyrin domain containing 3 (NLRP3) inflammasome may be a key target in the relationship between inflammation-mediated energy metabolism and metabolites of intestinal flora. Elucidating the relationship among the above three factors may help to identify new molecular targets for the prevention and treatment of HF and ultimately affect the course of HF. In this study, we systematically summarize evidence regarding the relationship among NLRP3 inflammasome, energy metabolism, intestinal microflora metabolites, and inflammation, as well as highlight advantages of NLRP3 inflammasome in treating HF.