Advances in the Study of NLRP3 in the Inflammatory Response to Exercise and Metabolic Syndrome

AMPK is an important regulator of cellular glycolipid metabolism and is in-volved in inflammation and oxidative stress in various diseases. AMPK is closely related to a family of nucleotide-binding oligomeric domain-like receptors, and activation of the AMPK signaling pathway prevents the assembly and activation of NLRP3 inflammatory vesicles, inflammatory vesicles are a series of protein complexes that mediate the maturation and release of the downstream inflammatory factors interleukin-18 (IL-18) and interleukin 1β (IL-1β), leading to apoptosis and causing a series of inflammatory responses. AMPK enhances cellular utilization of energy by activating oxidation and increasing uptake of glucose and fatty acids; there-fore, disruption of AMPK activity may lead to cellular Energy destruction and metabolic disorders leading to inflammation, which is involved in metabolic syndromes (MS) through various mechanisms, and inflammatory mechanisms have become an important research direction in the pathogenesis of MS; exercise has been shown to play a key role in regulating inflammation, but the mechanisms by which exercise regulates inflammatory vesicle activation are largely un-known. Therefore, investigating whether the effects of exercise on metabolic syndrome are mediated through AMPK-NLRP3 transduction mechanisms could provide a scientific rationale and new therapeutic targets for the treatment of metabolic diseases associated with inflammatory vesicles.