Atherosclerosis (As) is the pathological basis of a variety of common chronic cardiovascular and cerebrovascular diseases, which begins with the destruction of the natural barrier formed by the vascular endothelial cells. The main manifestations can change the signal transduction and related inflammatory gene expression of Caspase-1/Sirt1/AP-1, SREBP2/NOX2/NLRP3, KLF2/FoxP1/NLRP3, NFAT5/NLRP3 and thus activating endothelial cells. Then, monocytes infiltrate into the intima of aortic wall and differentiate into macrophages, resulting in an innate immune response in response to endothelial activation. Firstly, cholesterol crystallization in macrophages activates NLRP3/ASC/Caspase-1 inflammatory body pathway under the synergistic effect of other regulatory signals. It can increase the release of pro-inflammatory cytokines IL-1β and IL-18, mediate the expression of downstream inflammatory factors and chemokines, and promote the inflammatory response of As. Sustained chronic inflammatory reaction in vascular wall can change the phenotype of vascular smooth muscle cells, promote the formation of as plaque, change the composition of plaque and increase the vulnerability. Plaque microcalcification also increases the vascular stress at the plaque, with consequences that the risk of rupture is increased. In this paper, the research status of inflammatory mechanism of As, mediated by innate immune, can provide ideas for the development of anti-inflammatory drugs and promote the experimental design of anti-inflammatory research.