Type 2 diabetes and atherosclerosis have gradually garnered great attention as inflammatory diseases. Previously, the fact that Interleukin-1β (IL-1β) accelerates the development of type 2 diabetes and atherosclerosis has been proved in animal experiments and clinical trials. However, the continued studies found that the effect of IL-1β on type 2 diabetes and atherosclerosis is much more complicated than the negative impact. Nucleotide-binding oligomerization domain and leucine-rich repeat pyrin 3 domain (NLRP3) inflammasome, whose activation and assembly significantly affect the release of IL-1β, is a crucial effector activated by a variety of metabolites. The diversity of NLRP3 activation mode is one of the fundamental reasons for the intricate effects on the progression of type 2 diabetes and atherosclerosis, providing many new insights for us to intervene in metabolic diseases. This review focuses on how NLRP3 inflammasome affects the progression of type 2 diabetes and atherosclerosis and what opportunities and challenges it can bring us.
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