Skip to main content
. 2022 Feb 3;10:811196. doi: 10.3389/fcell.2022.811196

FIGURE 1.

FIGURE 1

Correlation between pyroptosis and progression of atherosclerotic plaques. Cholesterol crystal, and ox-LDL can activate inflammasomes in ECs, macrophages and VSMCs, trigger cellular pyroptosis and stimulate AS. Pyroptotic ECs can mediate T cell migration to the inner membrane and promote monocyte recruitment. Furthermore, pyroptotic ECs release proinflammatory cytokines, such as IL-18 and IL-1β, and result in vascular inflammation. Macrophages uptake cholesterol crystals and turn into lipid containing foam cells subsequently. Macrophage pyroptosis mediate the production of pro-inflammatory mediators and cytokines, including MMP, IL-18, and IL-1β. These pro-inflammatory mediators and cytokines also trigger foam cell pyroptosis, thereby forming the necrotic core of plaques in advanced lesions. Pyroptotic VSMCs release pro-inflammatory cytokines like IL-18 and IL-1β, and attenuate stability of fibrous caps via loss of collagen and matrix, causing inflammation, promoting plaque instability or erosion, and potentially worse AS. VSMCs, vascular smooth muscle cells. VECs, vascular endothelial cells. MMP, matrix metalloproteinase. IL-18, interleukin-18. IL-1β, interleukin-1β.