NLRP3 and atherosclerosis: In addition to LPS, under the pathological conditions of atherosclerosis, increased production of the metabolic product trimethylamine N-oxide (TMAO) by the gut microbiota can promote fosters leukocyte adherence and movement toward the vascular wall by upregulating the expression of cell adhesion molecules in ECs, as well as activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome to enhance inflammatory responses, thereby destabilizing atherosclerotic plaques (Wang C. et al., 2024).