Figure 3: Beneficial Effects of Extracellular Vesicles on Vascular Function

An increasing body of evidence points out the beneficial influence of certain EVs of diverse cellular sources in cardiovascular biology. This figure illustrates the favorable effects of EVs on endothelial and vascular function, atherosclerosis, and plaque stabilization. Endothelial EVs reduce endothelial apoptosis by inhibition of p38 activity mediated by an annexin I/phosphatidylserine receptor-dependent mechanism, contributing to endothelial protection. Moreover, endothelial EVs decrease endothelial regenerating cell apoptosis, facilitating endothelial repair. Platelet-derived MVs induce alterations in the endothelial-regenerating cell secretome toward a more proangiogenic profile and amplify vascular protection. Among the biological content transferred by EVs into target cells, miRNAs play a crucial role. Endothelial EVs promote vascular endothelial repair by inhibition of SPRED1 by delivering functional miRNA-126. Endothelial EVs promote anti-inflammatory effects by reducing endothelial ICAM-1 expression by the transfer of functional miRNA-222 into recipient cells. Exosomes from KLF-2-transduced or shear-stress-stimulated endothelial cells attribute to atheroprotection by transferring miRNA-143/145. Circulating leukocyte- and platelet-derived miRNA-223-containing exosomes penetrate the vascular wall, inhibit vascular smooth muscle cell proliferation and migration, resulting in decreased plaque size. Endothelial apoptotic bodies decrease vascular smooth muscle cell proliferation, limit plaque size, and increase plaque stability by miRNA-126-dependent inhibition of G-protein signaling (RGS16) pathway. MV = microvesicle; other abbreviations as in Figures 1 and 2.