Fig. 6 Interplay Among Peroxidation Products, Inflammation, and Immune Cell Recruitment in ACVD.  Oxidized mediators from PUFA metabolic pathways manifest as an accumulation of local eicosanoid outburst or “eicosanoid storms”, which further incorporate chemoattractant molecules. As a result, inflammatory mediators form the signaling basis for recruiting circulating immune cells, which in turn, propagates inflammatory signaling and hyperactivation of stress-responsive pathways in cardiac/arterial SMCs and endothelial cells. The combined action of active monocytes, inflammatory mediators, and signaling molecules exacerbates redox dysbalance and proliferative bias in atheroma microenvironments. Figure generated using  BioRender . JNK - jun N-terminal kinase; NRF-2 – nuclear factor erythroid-derived 2-like 2; PAR-1 – protease activated receptor-1; PPAR-γ - peroxisome proliferator activated receptor gamma; TLR4 – toll-like receptor 4. Fig. 6