scholarly journals The effect of trehalose administration on vascular inflammation in patients with coronary artery disease

2022 ◽  
Vol 147 ◽  
pp. 112632
Author(s):  
Tannaz Jamialahmadi ◽  
Farshad Emami ◽  
Ramin Khameneh Bagheri ◽  
Hedieh Alimi ◽  
Fabio Bioletto ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Vascular Inflammation ◽  
Artery Disease

Abstract 021: ARHGEF26 is a Novel Genetic Risk Factor for Vascular Inflammation and Coronary Artery Disease

2018 ◽  
Vol 38 (Suppl_1) ◽  
Author(s):  
Qiuyu M Zhu ◽  
Derek Klarin ◽  
Connor A Emdin ◽  
Mark Chaffin ◽  
Steven Horner ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Genetic Risk ◽  
Vascular Inflammation ◽  
Genetic Risk Factor ◽  
Artery Disease

scholarly journals Association of Interaction Between Smoking and CYP 2C19*3 Polymorphism With Coronary Artery Disease in a Uighur Population

2010 ◽  
Vol 16 (5) ◽  
pp. 579-583 ◽  
Author(s):  
Yi-Ning Yang ◽  
Xin-Lei Wang ◽  
Yi-Tong Ma ◽  
Xiang Xie ◽  
Zhen-Yan Fu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Vascular Inflammation ◽  
Multiple Logistic Regression Analysis ◽  
Rflp Analysis ◽  
Biologically Active ◽  
Pcr Rflp ◽  
Cyp2c19 Gene ◽  
Independent Risk Factors ◽  
Artery Disease

Objectives: Cytochrome P450 (CYP) 2C19 is expressed in vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which are potent endogenous vasodilators and inhibitors of vascular inflammation. The purpose of this study is to explore the relationship between the interaction of CYP2C19*3 polymorphism and smoking and coronary artery disease (CAD) in a Uighur population. Methods: In a Chinese Uighur case-control study of patients with CAD (n = 336) and healthy controls (n = 370), we investigated the roles of polymorphism in the CYP2C19 gene by the use of polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis. Results: The CYP2C19*3 AG + AA genotype was significantly more prevalent in patients with CAD (6.25.0% vs 2.96%; P = .03). Multiple logistic regression analysis showed 4 independent risk factors: the interaction of CYP2C19*3 and smoking (OR 7.22, 95% confidence interval [CI] 2.32-10.23; P = .009), smoking (OR 3.23, 95% CI 1.72-5.44; P = .003), blood sugar (OR 2.12, 95% CI 1.03-4.21; P < .01), and hypertension (OR 1.74, 95% CI 0.98-2.34; P = .013). Conclusions: The CYP2C19*3 polymorphism and CAD were synergistically and significantly associated in Chinese Uighur patients.

Vascular Inflammation and Angiographic Severity of Coronary Artery Disease in Young Asian Indians

2014 ◽  
Vol 5 (1) ◽  
pp. 15-21
Author(s):  
Imran Ahmed ◽  
Achyut Sarkar ◽  
Arindam Pande ◽  
Naveen Chandra GS ◽  
Shailesh Patil ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Asian Indians ◽  
Vascular Inflammation ◽  
Artery Disease

scholarly journals Functional investigation of the coronary artery disease gene SVEP1

2020 ◽  
Vol 115 (6) ◽  
Author(s):  
Michael J. Winkler ◽  
Philipp Müller ◽  
Amin M. Sharifi ◽  
Jana Wobst ◽  
Hanna Winter ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Vascular Inflammation ◽  
Missense Variant ◽  
Leukocyte Recruitment ◽  
Wild Type ◽  
Cellular Source ◽  
Elevated Expression ◽  
Artery Disease

AbstractA missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient (ApoE−/−Svep1+/−) compared to Svep1 wild-type mice (ApoE−/−Svep1+/+) and ApoE−/−Svep1+/− mice displayed elevated plaque neutrophil, Ly6Chigh monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in ApoE−/−Svep1+/− mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 (CXCL1) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in ApoE−/−Svep1+/− mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial CXCL1 expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency.

Role of Vascular Inflammation in Coronary Artery Disease: Potential of Anti-inflammatory Drugs in the Prevention of Atherothrombosis

2014 ◽  
Vol 15 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Daniel Medeiros Moreira ◽  
Roberto Leo da Silva ◽  
Jefferson Luís Vieira ◽  
Tammuz Fattah ◽  
Maria Emilia Lueneberg ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Vascular Inflammation ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Artery Disease

Toll–like receptor 4 gene Asp299Gly polymorphism is associated with reductions in vascular inflammation, angiographic coronary artery disease, and clinical diabetes

2004 ◽  
Vol 148 (6) ◽  
pp. 1034-1040 ◽  
Author(s):  
Matthew J. Kolek ◽  
John F. Carlquist ◽  
Joseph B. Muhlestein ◽  
Bryant M. Whiting ◽  
Benjamin D. Horne ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Vascular Inflammation ◽  
Clinical Diabetes ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Artery Disease

Platelet Transcriptional Profiling and Atherothrombosis

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. SCI-54-SCI-54
Author(s):  
Daniel I. Simon
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Apolipoprotein E ◽  
Odds Ratio ◽  
Cellular Proliferation ◽  
Vascular Inflammation ◽  
Case Control ◽  
Wild Type ◽  
Artery Disease

Abstract Platelets participate in events that immediately precede acute myocardial infarction. Because platelets lack nuclear DNA but retain megakaryocyte-derived mRNAs, the platelet transcriptome provides a novel window on gene expression preceding acute coronary events. We profiled platelet mRNA from patients with acute ST-segment–elevation myocardial infarction (STEMI, n=16) or stable coronary artery disease (n=44). The platelet transcriptomes were analyzed and single-gene models constructed to identify candidate genes with differential expression. We validated one candidate gene product by performing a prospective, nested case-control study (n=255 case-control pairs) among apparently healthy women to assess the risk of future cardiovascular events (nonfatal MI, nonfatal stroke, and cardiovascular death) associated with baseline plasma levels of the candidate protein. Platelets isolated from STEMI and coronary artery disease patients contained 54 differentially expressed transcripts. The strongest discriminators of STEMI in the microarrays were CD69 (odds ratio 6.2, P<0.001) and myeloid-related protein-14 (MRP-14 also known as S100A8/A9; odds ratio 3.3, P=0.002). In the validation study, the risk of a first cardiovascular event increased with each increasing quartile of MRP-8/14 (P trend <0.001) such that women with the highest levels had a 3.8-fold increase in risk of any vascular event (P<0.001). We evaluated vascular inflammation in wild-type and MRP-14-deficient (MRP-14-/-) mice that lack MRP-8/14 complexes with experimental arterial injury, vasculitis, or atherosclerosis. After femoral artery wire injury, MRP-14-/- mice had significant reductions in leukocyte accumulation, cellular proliferation, and neointimal formation compared with wild-type mice. In a cytokine-induced local Shwartzman-like reaction that produces thrombohemorrhagic vasculitis, MRP-14-/- mice had significant reductions in neutrophil accumulation, lesion severity, and hemorrhagic area. In response to high-fat feeding, mice doubly deficient in apolipoprotein E and MRP-8/14 complexes had attenuation in atherosclerotic lesion area and in macrophage accumulation in plaques compared with mice deficient in apolipoprotein E alone. These findings indicate that MRP-8/14 broadly regulates vascular inflammation and contributes to the biological response to vascular injury by promoting leukocyte recruitment. However, a causal role for MRP-14 in thrombosis has not been established and a viable molecular mechanism remains unknown. Here we show that time to thrombotic occlusion was prolonged markedly in MRP-14-/- mice. We observed that MRP-14 and MRP-8/14 are expressed in, and secreted by platelets, and that thrombus formation is reduced in whole blood from MRP-14-/- mice. Infusion of WT platelets or purified MRP-14 (or MRP-8/14) into MRP-14-/- mice shortened the carotid artery occlusion time, indicating that platelet-derived MRP-14 directly regulates thrombosis. Thus, a new pathway of inflammation and thrombosis involving MRP-14 is identified. MRP-14 represents a novel target for treating atherothrombotic disorders, including myocardial infarction and stroke. Disclosures: Simon: Cordis/J&J: Consultancy; Janssen/J&J: Consultancy; Medtronic Vascular: Consultancy; Merck: Consultancy; Medtronic Foundation: Research Funding.

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