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Circulating CD31+/Annexin V+ microparticles correlate with cardiovascular outcomes.

TLDR
The level of circulating CD31+/Annexin V+ MPs is an independent predictor of cardiovascular events in stable CAD patients and may be useful for risk stratification.
Abstract
Aims CD31+/Annexin V+ microparticles (MPs) are increased in patients with cardiovascular risk factors and impaired coronary endothelial function. We evaluated whether MPs are an independent marker for cardiovascular events in patients with stable coronary artery disease (CAD). Methods and results The number of CD31+/Annexin V+ MP was determined by flow cytometry in 200 patients (age 66.1 ± 10.4 years) and correlated with cardiovascular outcomes. The median follow-up time for major adverse cardiovascular and cerebral event (MACCE)-free survival was 6.1 (6.0/6.4) years. Four patients were lost to follow-up. A first MACCE occurred in 72 patients (37%). Microparticle levels were significantly higher in patients with MACCE compared with patients without event ( P = 0.004). The prevalence of diabetes ( P = 0.02) and male gender ( P = 0.05) was significantly related to the MP level. In multivariate analysis (cardiovascular risk factors, number of diseased vessels, use of angiotensin-converting enzyme-inhibitors and statins), high MP levels were associated with a higher risk for cardiovascular death [Hazard ratio (HR) 4.0, 95% confidence interval (CI) 1.1–14.6; P = 0.04], the need for revascularization (HR 2.4, 95% CI 1.3–4.4; P = 0.005), and the occurrence of a first MACCE (HR 2.3, 95% CI 1.4–3.8; P = 0.001). Inclusion of the MP level into a classical risk factor model substantially increased c -statistics from 0.637 (95% CI: 0.557–0.717) to 0.702 (95% CI: 0.625–0.780) ( P = 0.03). Conclusion The level of circulating CD31+/Annexin V+ MPs is an independent predictor of cardiovascular events in stable CAD patients and may be useful for risk stratification.

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Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I

TL;DR: This review will focus on the most current advances in the pathophysiological mechanisms of vascular disease: emerging role of endothelium in obesity-induced insulin resistance, hyperglycemia-dependent microRNAs deregulation and impairment of vascular repair capacities, and alterations of coagulation, platelet reactivity, and microparticle release.
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Rho-associated coiled-coil containing kinases (ROCK): Structure, regulation, and functions

Linda Julian, +1 more
- 12 Dec 2014 - 
TL;DR: The structure, regulation, and functions of ROCK are focused on and two mammalian ROCK homologs have been identified, ROCK1 and ROCK2, hereafter collectively referred to as ROCK.
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Extracellular vesicles in coronary artery disease

TL;DR: Current knowledge on the role of extracellular vesicles in coronary artery disease, and their emerging potential as biomarkers and therapeutic agents are summarized.
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Microparticles, Vascular Function, and Atherothrombosis

TL;DR: High levels of MPs circulate in the blood of patients with atherothrombotic diseases, where they could serve as a useful biomarker of vascular injury and a potential predictor of cardiovascular mortality and major adverse cardiovascular events.
Journal ArticleDOI

Microparticles: biomarkers and beyond.

TL;DR: The present review examines the evidence for microparticles as both biomarkers of, and contributors to, the progression of disease and novel concepts relating to the formation of microparticle and their biological effects are examined.
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Endothelial Dysfunction, Oxidative Stress, and Risk of Cardiovascular Events in Patients With Coronary Artery Disease

TL;DR: Data support the concept that oxidative stress may contribute not only to endothelial dysfunction but also to coronary artery disease activity, and predict the risk of cardiovascular events in patients with coronary arteries disease.
Journal ArticleDOI

Membrane blebbing during apoptosis results from caspase-mediated activation of ROCK I

TL;DR: It is shown that the Rho effector protein ROCK I, which contributes to phosphorylation of myosin light-chains, myOSin ATPase activity and coupling of actin–myosin filaments to the plasma membrane, is cleaved during apoptosis to generate a truncated active form.
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