Simvastatin attenuates the endothelial pro-thrombotic shift in saphenous vein grafts induced by Advanced glycation endproducts

Spadaccio, Cristiano; Marco, Federico De; Domenico, Fabio Di; Coccia, Raffaella; Lusini, Mario; Barbato, Raffaele; Covino, Elvio; Chello, Massimo

doi:10.1016/j.thromres.2013.12.023

Cited by 11 publications

(9 citation statements)

References 41 publications

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“…Other studies illustrated that HMGB1 binds to platelets and that platelet activation resulted in upregulation of RAGE expression and that HMGB1 was highly expressed in platelet-rich human coronary artery thrombi (87). In ECs obtained from human saphenous veins, incubation with AGEs increased neutrophil adhesion and generation of reactive oxygen species (ROS) and treatment with simvastatin reduced these prothrombotic stimuli and reduced RAGE expression (88). ECs from diabetic patients treated with simvastatin resulted in reduced expression of RAGE, neutrophil adhesion and ROS (88).…”

Section: Studies In Human Subjectsmentioning

confidence: 99%

“…In ECs obtained from human saphenous veins, incubation with AGEs increased neutrophil adhesion and generation of reactive oxygen species (ROS) and treatment with simvastatin reduced these prothrombotic stimuli and reduced RAGE expression (88). ECs from diabetic patients treated with simvastatin resulted in reduced expression of RAGE, neutrophil adhesion and ROS (88). However, other studies tested if the levels of platelet HMGB1 were associated with outcomes in symptomatic CAD.…”

Section: Studies In Human Subjectsmentioning

confidence: 99%

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Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models

Egaña-Gorroño

López‐Díez

Yepuri

et al. 2020

Front. Cardiovasc. Med.

156

135

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Section: Studies In Human Subjectsmentioning

confidence: 99%

Section: Studies In Human Subjectsmentioning

confidence: 99%

Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models

Egaña-Gorroño

López‐Díez

Yepuri

et al. 2020

Front. Cardiovasc. Med.

156

135

View full text Add to dashboard Cite

show abstract

“…MK also known as simvastatin treatment of hypercholesterolemic mice and monkeys reduced oxLDL, monocyte procoagulant protein tissue factor (TF) expression, microparticle TF activity, activation of coagulation, and inflammation, without affecting total cholesterol levels [28]. MK decreased the rise in neutrophil adhesion and ROS generation following stimulation of saphenous vein endothelial cell culture with advanced glycation end products in vitro and in vivo data from diabetic patients administered with MK showed a similar significant reduction in neutrophil adhesion and ROS generation [29]. As far we know, there is no report about MA effect on leukocytes.…”

Section: Discussionmentioning

confidence: 99%

<b><i>Monascus Adlay</i></b> and Monacolin K Attenuates Arterial Thrombosis in Rats through the Inhibition of ICAM-1 and Oxidative Stress

Tien¹,

Chueh²,

Hsia³

et al. 2016

Kidney Blood Press Res

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Background/Aims: Monascus Adlay (MA) prepared from fungal fermentation of Monascus purpureus inoculating with cooked adlay contains high content of monakolin K (MK) and phenolic compounds. We explored whether MA and MK improve FeCl₃-induced arterial thrombosis in rats. Methods: The rats were divided into control, FeCl₃-treated rat carotid artery occlusion (TTO), TTO determined with one-week MA, and TTO determined with one-week MK. We compared MA or MK effects on oxidative stress by chemiluminescence amplification and immunohistochemistry, TTO by a transonic system, NFκB, ICAM-1, endoplasmic reticulum stress CHOP and Nrf2 signaling by western blotting. Results: MA or MK efficiently depressed O₂^-, H₂O₂ and HOCl levels, platelet activation and aggregation and H₂O₂-enhanced ICAM-1 and VCAM-1 expression in the endothelial cells. FeCl₃ significantly increased NFκB p65, 3-nitrotyrosine, CHOP and ICAM-1 expression, and decreased nuclear Nrf2 translocation and induces arterial thrombus formation. MA or MK pretreatment significantly elongated the level of FeCl₃-induced TTO compared to TTO group, significantly decreased proinflammatory NF-κB/ICAM-1 signaling, endoplasmic reticulum stress CHOP expression and decreased thrombotic area. MA or MK significantly preserved nuclear Nrf2 translocation. MA and MK exerted a similar protective effect in attenuating thrombus formation. Conclusions: We suggest MA is better than MK to improve FeCl₃-induced arterial thrombosis.

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“…Simvastatin was also shown to inhibit the endothelial prothrombotic shift in the SVG in patients with well-controlled diabetes. 83 A post-CABG follow-up study of 1 to 11 years in length showed that active reduction in the LDL-C level reduced the development of atherosclerosis in the SVG. 80 Kang et al.…”

Section: Drug Preventionmentioning

confidence: 99%

Review of risk factors, treatment, and prevention of saphenous vein graft disease after coronary artery bypass grafting

Gao

Yin

2018

J Int Med Res

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Saphenous vein graft disease (SVGD) is a type of vascular disease that may develop after coronary artery bypass grafting (CABG). SVGD seriously affects the short-term and long-term effects of CABG and increases the incidence of major adverse cardiovascular events. It is very important to identify patients at greatest risk and carry out prevention and treatment measures to determine the risk factors for SVGD. Many factors contribute to SVGD when the vein is grafted into an arterial environment, such as surgery-related factors, smoking, diabetes mellitus, hyperlipidemia, and others. In this review, we discuss the risk factors for SVGD, current surgical and pharmacologic therapies with which to manage SVGD, and the prevention of SVGD.

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Simvastatin attenuates the endothelial pro-thrombotic shift in saphenous vein grafts induced by Advanced glycation endproducts

Cited by 11 publications

References 41 publications

Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models

Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models

<b><i>Monascus Adlay</i></b> and Monacolin K Attenuates Arterial Thrombosis in Rats through the Inhibition of ICAM-1 and Oxidative Stress

Review of risk factors, treatment, and prevention of saphenous vein graft disease after coronary artery bypass grafting

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