We hypothesise that IPE attenuates priming and activation of the NLRP3 inflammasome in monocyte-derived macrophages, thereby reducing cellular inflammation and senescence.<h4>Conclusions</h4>This study will provide mechanistic insight into how IPE influences macrophage-driven inflammation in ASCVD and T2DM, informing strategies to target residual inflammatory risk in high-risk cardiometabolic populations. Here, NLRP3 is linked to atherosclerosis.