Figure 1.

Throughout the various stages of atherosclerosis, exosomes from various cells facilitate the progression of the disease. Upon early fatty streak formation, exosomes from activated monocytes provide endothelial cells with adhesion molecules which enable recruitment of more monocytes and leukocytes to the site. As the fatty streak develops into an intermediate lesion, fat laden macrophages (foam cells) release exosomes which can supply embryonic type integrins to vascular smooth muscle cells (VSMCs) to allow their migration to the injured site. Further progression into a fibrous plaque coincides with an increase in exosome release from monocytes and macrophages which particularly target endothelial cells. This results in angiogenesis and further permeability of endothelial cells, eventually leading to the exposure of the collagenous cap into the arterial lumen. Subsequent platelet aggregation and clot formation is supported by exosomes secreted from platelets and VSCMs which target endothelial cells. Noting the important role of exosomes in the progression of atherosclerosis may provide further insight into specific characterization of the atherosclerotic stage, key molecular players involved in the pathophysiology of the disease, and more targeted therapeutic processes.