Effects of Ezetimibe on Endothelial Progenitor Cells and Microparticles in High-Risk Patients

Lins, Lívia Campos Amaral; França, Carolina Nunes; Fonseca, Francisco Antônio Helfenstein; Barbosa, Simone P.; Matos, Lívia Nascimento de; Aguirre, Ana Carolina Carneiro; Bianco, Henrique Tria; Amaral, Jônatas Bussador do; Izar, Maria Cristina de Oliveira

doi:10.1007/s12013-014-9973-9

Cited by 23 publications

(13 citation statements)

References 34 publications

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“…92 . A lack of effect on microparticles and endothelial progenitor cells by ezetimibe treatment was reported also in patients at high-risk for coronary heart disease 93 . The Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial has been designed to assess the effects of long-term (4.3 years) treatment with ezetimibe+simvastatin in patients with asymptomatic, mild-to-moderate aortic-valve stenosis 96 (Table 2).…”

Section: Inhibition Of Npc1l1 By Ezetimibe and Inflammationmentioning

confidence: 88%

Niemann-Pick C1-Like 1 (NPC1L1) Inhibition and Cardiovascular Diseases

Pirillo¹,

Catapano²,

Norata³

2016

CMC

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Circulating levels of cholesterol derive from either endogenous production or intestinal absorption of dietary and biliary cholesterol. Niemann-Pick C1-Like 1 (NPC1L1) is a transmembrane protein that plays a key role in the intestinal absorption of cholesterol by facilitating its uptake through vesicular endocytosis. NPC1L1 is the molecular target of ezetimibe which binds its extracellular loop and inhibits sterol absorption without affecting the absorption of other molecules. Ezetimibe significantly reduces plasma levels of total and low density lipoprotein cholesterol (LDL-C) as monotherapy or when added to statins, the association with a low dose of statin is of particular interest for patients experiencing statin-related side effects. The recent results of the IMPROVE-IT study, which evaluated the cardiovascular effect of ezetimibe added to simvastatin therapy in subjects who had had an acute coronary syndrome and with LDL-C levels within the recommended range, showed that a further LDL-C lowering reduced the incidence of cardiovascular events. To date, ezetimibe represents the only inhibitor of NPC1L1 available for clinical use, however, novel amino-ß-lactam ezetimibe derivatives have been synthesized and their efficacy to inhibit NPC1L1 protein and decrease plasma cholesterol levels is under evaluation.

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Section: Inhibition Of Npc1l1 By Ezetimibe and Inflammationmentioning

confidence: 88%

Niemann-Pick C1-Like 1 (NPC1L1) Inhibition and Cardiovascular Diseases

Pirillo¹,

Catapano²,

Norata³

2016

CMC

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“…It has been reported on the basis of bulk analysis that the total amounts of EVs of different sizes and origins are elevated in patients with higher cardiovascular risk scores [11], endothelial dysfunction [34–36], ischemic stroke [12,37], stable atherosclerotic plaques [13,38], and acute coronary syndromes [15,21,22,39–43]. Moreover, it has been shown that EV levels correlate with clinical outcomes in patients with coronary artery disease [44,45] and are reduced with statin therapy [46,47]. …”

Section: Discussionmentioning

confidence: 99%

Flow analysis of individual blood extracellular vesicles in acute coronary syndrome

et al. 2016

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A diverse population of small extracellular vesicles (EVs) that are released by various cells has been characterized predominantly in bulk, a procedure whereby the individual characteristics of EVs are lost. Here, we used a new nanotechnology-based flow cytometric analysis to characterize the antigenic composition of individual EVs in patients with acute coronary syndrome (ACS). Plasma EVs were captured with 15-nm magnetic nanoparticles coupled to antibodies against CD31 (predominantly an endothelial marker), CD41a (a marker for platelets), and CD63 or MHC class I (common EV markers). The total amounts of EVs were higher in the ACS patients than in the controls, predominantly due to the contribution of patients with acute myocardial infarction. For all captured fractions, the differences in the EV amounts were restricted to CD41a+ EVs. The increase in the numbers of EVs in the ACS patients, predominantly of platelet origin, probably reflects platelet activation and may indicate disease progression.

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“…However, some authors did not observe such effect of statins [96,97], and, as discussed in the 2019 ESC/EAS Guidelines for the management of dyslipidemias, the clinical relevance of the pleiotropic effects of statins remains clinically unproven [98], and thus may be object of future research.…”

Section: Pharmacological Treatment Of Dyslipidemia and Circulating MVmentioning

confidence: 97%

Cross-Talk between Lipoproteins and Inflammation: The Role of Microvesicles

Chiva‐Blanch

Badimon

2019

JCM

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Atherothrombosis is the principal underlying cause of cardiovascular disease (CVD). Microvesicles (MV) are small blebs originated by an outward budding at the cell plasma membranes, which are released in normal conditions. However, MV release is increased in pathophysiologic conditions such as CVD. Low density lipoprotein (LDL) and MV contribute to atherothrombosis onset and progression by promoting inflammation and leukocyte recruitment to injured endothelium, as well as by increasing thrombosis and plaque vulnerability. Moreover, (oxidized)LDL induces MV release and vice-versa, perpetuating endothelium injury leading to CVD progression. Therefore, MV and lipoproteins exhibit common features, which should be considered in the interpretation of their respective roles in the pathophysiology of CVD. Understanding the pathways implicated in this process will aid in developing novel therapeutic approaches against atherothrombosis.

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Effects of Ezetimibe on Endothelial Progenitor Cells and Microparticles in High-Risk Patients

Cited by 23 publications

References 34 publications

Niemann-Pick C1-Like 1 (NPC1L1) Inhibition and Cardiovascular Diseases

Niemann-Pick C1-Like 1 (NPC1L1) Inhibition and Cardiovascular Diseases

Flow analysis of individual blood extracellular vesicles in acute coronary syndrome

Cross-Talk between Lipoproteins and Inflammation: The Role of Microvesicles

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