Abstract
The levels of circulating microparticles (MPs) are raised in various cardiovascular diseases. Their increased level in plasma is regarded as a biomarker of alteration in vascular function. The prominent MPs present in blood are endothelial microparticles (EMPs) described as complex submicron (0.1 to 1.0 μm) vesicles like structure, released in response to endothelium cell activation or apoptosis. EMPs possess both physiological and pathological effects and may promote oxidative stress and vascular inflammation. EMPs release is triggered by inducer like angiotensin II, lipopolysaccharide, and hydrogen peroxide leading to the progression of atherosclerosis. However, there are multiple physiological pathways for EMPs generation like NADPH oxidase derived endothelial ROS formation, Rho kinase pathway, and mitogen-activated protein kinases. Endothelial dysfunction is a key initiating event in atherosclerotic plaque formation. Atheroemboli, resulting from ruptured carotid plaques, is a major cause of stroke. Increasing evidence suggests that EMPs play an important role in the pathogenesis of cardiovascular disease, acting as a marker of damage, either exacerbating disease progression or triggering a repair response. In this regard, it has been suggested that EMPs have the potential to act as biomarkers of disease status. This review aims to provide updated information of EMPs in relation to atherosclerosis pathogenesis.
Highlights
What Are Microparticles?Microparticles (MPs) are cell membrane-shedded submicron fragments ranging from 0.1 to 1.0 μm containing information like mRNA, microRNAs (miRNAs), receptor, and specific proteins of parent cell
The levels of circulating microparticles (MPs) are raised in various cardiovascular diseases
endothelial microparticles (EMPs) release is triggered by inducer like angiotensin II, lipopolysaccharide, and hydrogen peroxide leading to the progression of atherosclerosis
Summary
Microparticles (MPs) are cell membrane-shedded submicron fragments ranging from 0.1 to 1.0 μm containing information like mRNA, microRNAs (miRNAs), receptor, and specific proteins of parent cell. MPs have been identified as membrane vesicles released from blood-related cells such as endothelial cells, smooth muscle cells, platelets, erythrocytes, and leukocytes, as recognized by their specific surface proteins [2, 3]. It is clear that MPs formation and shedding involve reconstitution of cell membrane phospholipid structure, with outer leaflet subjected to phosphatidylserine (PS), and alteration of the cell architecture, with the disruption of cytoskeleton organization [6,7,8,9]. Several studies report the existence of small vesicles similar in size as MPs but do not expose PS in the outer leaflet. The area of MP study is rapidly growing as the role of MPs in the pathogenesis of diabetes mellitus [10], lungs cancer [11, 12], central nervous system disorder [13], inflammation [14, 15], systemic lupus erythematosus [16], and cardiovascular diseases (CVDs) [17] has been highlighted by various clinical and experimental research
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