Platelet-derived vesicles: diagnostic and predictive value in cardiovascular diseases

Abstract

There is emerging evidence that endogenous microvesicles released by platelets may play a pivotal role in pathogenesis of numerous diseases including stable and unstable ischemic heart disease, atherosclerosis, hypertension, idiopathic pulmonary hypertension, atrial fibrillation/flutter, acute and chronic heart failure, as well as systemic vasculitis, systemic lupus erythematosus, antiphospholipid syndrome, transplant rejection, diabetes-induced angiopathy. Microvesicles that leased from the platelets exist as cargo for a large of number biological-active molecules including regulatory peptides, hormones, growth factors, active molecules coordinating cell-to-cell cooperation. Moreover, platelet-derived microvesicles are concerned about a conspicuous component in regulating angiogenesis, cardiac protection, and vascular repair. Recent animal and clinical studies have shown that the number of circulating platelet-derived microvesicles may sufficiently increase in accelerating atherosclerosis, acute atherothrombotic events, i.e., recurrent ischemia, myocardial infarction, thrombosis, hypertension, and stroke, microvascular inflammation. It is suggested that exaggerating levels of circulating platelet-derived microvesicles is strongly associated with endothelial dysfunction. The review is discussed the role of platelet-derived vesicles in the pathogenesis of the cardiovascular disease, as well as diagnostic and predictive capabilities of platelet-derived vesicles as biomarkers of a natural evolution of the diseases.

Extracellular Endothelial Cell-Derived Vesicles: Emerging Role in Cardiac and Vascular Remodeling in Heart Failure

“…Previous clinical studies have shown that there were no significant differences in the circulating number of EVs derived from platelets (CD41a+), neutrophils (CD66b+), erythrocytes (CD235a+), monocytes (CD14+), T lymphocytes (CD3+), and B lymphocytes (CD19+) between healthy volunteers and HF patients (56). In contrast, a decreased number of circulating endothelial cells (CD31+CD41a-) EVs was found in HF patients (57). However, the total number of EVs enriched phosphatidylserines was significantly increased in HF patients compared with healthy volunteers (56).…”

Ultrastructural Study of Platelet Behavior and Interrelationship in Sprouting and Intussusceptive Angiogenesis during Arterial Intimal Thickening Formation

“…Platelet participation in several pathophysiological mechanisms involved in atherosclerosis, bypass stenosis, and restenosis is an important subject of research in human and experimental pathology [ 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 ]. Platelets act in angiogenesis [ 15 , 16 , 17 , 18 ], which is one of the main pathophysiological mechanisms of this pathology.…”

Human Platelets Take up Anti-VEGF Agents

“…As already pointed out by Berezin et al and Gasecka et al, platelets are the main source of extracellular vesicles in plasma, which are the cargo for a large number of biologicalactive molecules including cytokines, chemokines, hormones, enzymes, growth factors, and their receptors (e.g., VEGF), as well as adhesion receptors coordinating cell-tocell interactions [50,51]. ey contribute to numerous biological mechanisms such as microvascular inflammation, atherosclerotic plaque shaping and rupture, endothelial dysfunction, angiogenesis, neovascularization, thrombosis, cardiac remodeling, and kidney dysfunction [52][53][54][55][56][57].…”