The risk of cardiovascular events caused by acute thrombosis is high, including acute myocardial infarction, acute stroke, acute pulmonary embolism, and deep vein thrombosis. In this review, we summarize the roles of extracellular vesicles of different cellular origins in various cardiovascular events associated with acute thrombosis, as described in the current literature, to facilitate the future development of a precise therapy for thrombosis caused by such vesicles. We hope that our review will indicate a new horizon in the field of cardiovascular research with regard to the treatment of acute thrombosis, especially targeting thrombosis caused by extracellular vesicles secreted by individual cells. As more emerging technologies are being developed, new diagnostic and therapeutic strategies related to EVs are expected to be identified for related diseases in the future.

Background and Objectives With the growing incidence of acute myocardial infarction (MI), angiogenesis is vital for cardiac function post-MI. The role of bone marrow mesenchymal stem cells (BMSCs) in angiogenesis has been previously confirmed. Irisin is considered a potential vector for angiogenesis. The objective of the present study was to investigate the potential role of irisin in the angiogenesis of BMSCs. Methods and Results In vivo , irisin-treated BMSCs (BMSCs＋irisin) were transplanted into an MI mouse model. On day 28 post-MI, blood vessel markers were detected, and cardiac function and infarct areas of mice were evaluated. In vitro , paracrine effects were assessed by examining tube formation in human umbilical vein endothelial cells (HUVECs) co-cultured with the BMSCs＋irisin supernatant. The scratch wound-healing assay was performed to evaluate HUVEC migration. Western blotting was performed to determine PI3k/Akt pathway activation in the BMSCs＋irisin group. Transplantation of BMSCs＋irisin promoted greater angiogenesis, resulting in better cardiac function in the MI mouse model than in controls. In the BMSC＋irisin group, HUVECs demonstrated enhanced tube formation and migration. Activation of the PI3k/Akt pathway was found to be involved in mediating the role of irisin in the angiogenesis of BMSCs. Conclusions In cardiovascular diseases such as MI, irisin administration can enhance angiogenesis of BMSCs and promote cardiac function via the PI3k/Akt pathway, optimizing the therapeutic effect based on BMSCs transplantation.