Fig. 1 Genesis, Progression and Evolution of Arterial Atherosclerotic Plaque.  Early stages of lesion formation involves LDL infiltration and accumulation on the arterial walls, followed by multiple steps of oxidative modification and inflammatory responses in the arterial microenvironment. Mononuclear cells (PBMC) including macrophages and cytotoxic T-lymphocytes (CTL) circulating in the bloodstream respond to the chemoattractant stimuli by adhering and migrating into the intima. Subsequent mediator release by PBMC in the intima promotes smooth muscle cell (SMC) migration and initiates atheroma growth. Following genesis, the atheroma undergoes complex modifications encompassing proliferation, pro-inflammatory signaling, cell death of SMC and PBMC, and activated platelets in the vicinity. Along with lipid particles, these cellular masses accumulate to form a necrotic fibro-fatty lesion core, which leads to further inflammation and obstruction of arterial flow. Once the lesion core approaches critical mass, the fibrotic cap of the core ruptures and initiates one of a set of possible pathways. The rupture can be healed with fibrinolytic (red) or platelet-rich (white) thrombus formation with the help of tissue growth factors that can further exacerbate arterial blockage and/or the rupture can cause a severe inflammatory response in thrombosis sites leading to ischemic damage and further complications. Figure generated using  BioRender . (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.) Fig. 1