NLRP3 and atherosclerosis: Most studies showed that monocytes promote phenotypic switching of VSMCs through activation of NLRP3 inflammasome, which exerted a likely detrimental role in the plaque stability in humans.154 In addition, mitochondrial dysfunction, oxidative stress, lysosome rupture, and endoplasmic reticulum (ER) stress as well as extracellular Ca2+, which are involved in activation of inflammasome, all existed in the plaques, especially in necrotic cores, and however, few studies have been conducted on these mechanisms in atherosclerosis.191