Microparticles and their role in coronary artery disease

Abstract

Despite significant advances in prevention, medical and interventional management, coronary artery disease (CAD) remains the leading cause of death worldwide. Although the number of people being diagnosed with CAD has plateaued in the western world, it is projected to increase significantly in the developing world reaching epidemic proportions, particularly in South Asia. To better stratify the risk of developing and suffering a cardiovascular event due to CAD, not only plasma biomarkers relating to disease burden but also disease activity in CAD are needed; this will allow targeting of appropriate management to high-risk patients for acute events. Over the last twenty years, data have emerged showing the role of sub-micron vesicles called microparticles (MPs) in the pathogenesis of formation and evolution of atherosclerotic plaques causing either stable angina (SA) or acute coronary syndromes (ACS). Herein we provide an overview of our current knowledge of MP formation, composition and possible mechanisms through which they could be contributing to CAD. We also reviewed currently available methods and their limitations in quantifying MPs and in determining their functional aspects. Role of various treatments ranging from dietary substitutes to oral medicines and intravenous medications to mechanistic procedures such as hemofiltration are elaborated. Although evidence implicating the role of MPs in CAD are mounting large scale prospective studies are still lacking and are the need of the hour prior to establishing the use of MPs as biomarkers for the early detection of CAD and its progression.

Circulating microparticle concentrations across acute and chronic cardiovascular disease conditions

“…Cardiovascular disease (CVD) is expected to affect over 40% of adults in the United States by 2030 (Heidenreich et al, 2011). With only half of CV events explained by traditional CVD risk factors (Mora, Cook, Buring, Ridker, & Lee, 2007), biomarkers that extend beyond traditional risk factors may be critical to explain CVD activity (Koganti et al, 2017). Cellular endothelial microparticles (MPs) have emerged as novel biomarkers and may serve in a clinical capacity to identify CVD burden (Markiewicz, Richard, Marks, & Ludwicka-Bradley, 2013).…”

Effects of HIV-1 gp120 and TAT-derived microvesicles on endothelial cell function

“…Indeed, both gp120 and Tat have been shown to activate various signaling proteins involved in EMV formation and release. For example, gp120 binding of CCR5 and/or CXCR4 (30) results in the activation of p38 mitogen-activated protein kinase (MAPK) and caspase-2 (18,40), key initiators of EMV formation and release under conditions of cell activation and increased apoptotic susceptibility (27,41). p38 MAPK activation and caspase-2 provoke cytoskeletal rearrangement, stimulate microvesicle vesiculation, and initiate release (41).…”

Current advances in circulating inflammatory biomarkers in atherosclerosis and related cardio‐cerebrovascular diseases

“…The association between MPs and AS is mediated by multiple mechanisms including inflammatory response, endothelial dysfunction, angiogenesis, and coagulation. 44 , 45 …”