Microvesicles as Emerging Biomarkers and Therapeutic Targets in Cardiometabolic Diseases

Abstract

Microvesicles (MVs, also known as microparticles) are small vesicles that originate from plasma membrane of almost all eukaryotic cells during apoptosis or activation. MVs can serve as extracellular vehicles to transport bioactive molecules from their parental cells to recipient target cells, thereby serving as novel mediators for intercellular communication. Importantly, more and more evidence indicates that MVs could play important roles in early pathogenesis and subsequent progression of cardiovascular and metabolic diseases. Elevated plasma concentrations of MVs, originating from red blood cells, leukocytes, platelets, or other organs and tissues, have been reported in various cardiometabolic diseases. Circulating MVs could serve as potential biomarkers for disease diagnosis or therapeutic monitoring. In this review, we summarized recently-published studies in the field and discussed the role of MVs in the pathogenesis of cardiometabolic diseases. The emerging values of MVs that serve as biomarker for non-invasive diagnosis and prognosis, as well as their roles as novel therapeutic targets in cardiometabolic diseases, were also described.

Keywords: Biomarker; Cardiometabolic disease; Exosome; Microparticle; Microvesicle.

Figure 1

Extracellular vesicles Schematic depiction of the extracellular vesicles, including exosomes, microvesicles, and apoptotic bodies. Exosomes are smaller luminal vesicles (30–100 nm in diameter) originating from intracellular endosomes. Microvesicles (also called microparticles) are small membrane vesicles (0.1–1 μm in diameter) released from cell membrane surface during activation or apoptosis of all eukaryotic cells. Apoptotic bodies (1–5 µm in diameter) are released from cell membrane surface in late stage of apoptosis of all cell types.

Figure 2

Mechanisms underlying the involvement of extracellular vesicles in pathologies of cardiometabolic diseases The potential pathogenic mechanisms of microvesicles underlying coagulation, vascular dysfunction, inflammation, insulin resistance, and cardiomyocyte injury are illustrated. The exposure of EVs to tissue factor and phosphatidylserine could be involved in coagulation cascade and increase the risk of thrombosis in cardiovascular disease and diabetic complications. EVs derived from apoptotic cells have proinflammatory properties by inducing the exposure of adhesion molecules to plasma membrane and secretion of cytokines that are important in atherogenesis and adipose inflammation, thereby contributing to pathogenesis of cardiometabolic diseases. EVs could also directly impair insulin signaling pathways, thus contributing to insulin resistance and metabolic syndrome. The mechanism of vascular dysfunction induced by EVs could be associated with the decreased production of nitric oxide and prostacyclin in the endothelial cells. In addition, EVs could directly affect cardiomyocytes by inducing apoptosis, therefore maybe involved in cardiomyocyte injury and heart damage. EV, extracellular vesicle.