The chain of events initiated by MPs on atherosclerosis physiopathology. Endothelial microparticles (EMPs) and platelet microparticles (PMPs) are generated by the activation of endothelium with a number of factors like smoking, oxidative stress, obesity, and high blood pressure whereas monocyte-microparticles (MMPs) are generated by proinflammatory cytokines (tumor necrosis factor-α, interleukin 1-β), cigarette smoking, and C-reactive protein (CRP). EMPs can activate vascular smooth muscle cells (VSMCs) to express matrix metalloproteinase-9 (MMP-9) that can degrade elastic lamina barrier to facilitate VSMC migration from tunic media to tunic intima at the site of atherosclerotic lesion. Furthermore, EMPs also upregulate ERK, JNK, and p38 through MAPKs pathway leading to proliferation and migration of VSMC to develop atheroma plaque. Cell adhesion molecules expressed by EMPs and PMPs facilitate leukocytes and platelets adhesion to the endothelial surface thereby developing intimal thickening and vascular lesion. MMPs can activate inducible nitric oxide synthase pathway to release nitric oxide (NO) and procoagulant responsible for vascular inflammation and endothelial dysfunction. Collectively, all this event leads to atherosclerosis.