Structural Characterization, Molecular Docking and Protective Effect on Coronary Artery Disease of a New Nanostructured Cu(II)-Coordination Polymer by Reducing the Inflammatory Level

2020 ◽  
Vol 30 (9) ◽  
pp. 3617-3625
Author(s):  
Zhen Liu ◽  
Yi Li ◽  
Fengquan Dong ◽  
Haiying Li ◽  
Lei Zhou
2007 ◽  
Vol 97 (03) ◽  
pp. 458-463 ◽  
Author(s):  
Zsuzsanna Bereczky ◽  
Éva Katona ◽  
Róza Ádány ◽  
László Muszbek ◽  
Zoltán Vokó

SummarySeveral studies suggested that Val34Leu variant of factor XIII (FXIII) might have a protective effect against coronary artery disease (CAD), but studies not supporting these findings have also been published. The authors performed a meta-analysis of 16 studies on 5,346 cases and 7,053 controls that investigated the association between Val34Leu polymorphism and CAD defined as history of myocardial infarction or significant stenosis on a coronary artery assessed by coronary angiography. Because of the heterogeneity of the study-specific results, the pooled effect estimates were calculated by a random-effects empirical Bayes model. The combined odds ratios for CAD were 0.82 (95% confidence interval [95% Cl] 0.73, 0.94) for the heterozygotes of the FXIIIVal34Leu variant, 0.89 (95% CI 0.69, 1.13) for the homozygotes, and 0.81 (95% CI 0.70, 0.92) for the heterozygotes and homozygotes combined. The results were essentially the same when only myocardial infarction was considered as outcome. The beneficial effect of the polymorphism might be smaller than the effect estimates obtained in this metaanalysis, because the analysis raised the possibility of publication bias. Data published in the literature suggest that gene-gene and gene-environmental interactions might significantly influence the protective effect of FXIII-AVal34Leu polymorphism.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Christoph R Sinning ◽  
Edith Lubos ◽  
Renate Schnabel ◽  
Jan-Malte Sinning ◽  
Philipp S Wild ◽  
...  

Introduction: Selenium is an essential trace element with important antioxidative properties. The aim of this study was to evaluate the relative risk of cardiovascular mortality according to increasing concentrations of selenium and a possible protective effect of high selenium concentrations against oxidative stress in patients with established coronary artery disease. Methods: In this substudy of the prospective Athero Gene survey, 1867 patients were included. These patients could be stratified according to the diagnosis into stable angina pectoris (SAP, n=852), acute coronary syndrome (ACS, n=879) and exclusion of relevant coronary artery disease (NoCAD, n=123). Results: Low selenium concentration is associated with an increased relative risk for cardiovascular mortality. When the collective with ACS is stratified into tertiles of rising selenium concentration, the survival curves according to the Kaplan-Meier-Method (Log-Rank Test: P=0.0001) reveal an adverse outcome. In contrast, in patients with SAP was no association between the selenium concentration and outcome (P=0.35) had been observed. In a fully adjusted Cox proportional hazards model encompassing classical risk factors, medication and laboratory markers, thirds of increasing selenium concentration were associated with a protective effect in patients with ACS (tertiles: HR: 0.362, 95% CI: 0.149–0.878, P=0.025). In a Cox backward-stepwise regression analysis encompassing sixteen variables of cardiovascular risk prediction, one increment increase in selenium concentration decreased the risk of cardiovascular mortality in patients with ACS (HR:0.746, 95%CI: 0.602–0.926; P-Value: 0.008). Conclusion : Increased selenium concentration is related to an improved outcome after the acute event. This data encourages the concept of selenium administration in patients with ACS.


2006 ◽  
Vol 52 (4) ◽  
pp. 243-246 ◽  
Author(s):  
Marina Kardara ◽  
Athanasia Papazafiropoulou ◽  
Paraskevi Katsakiori ◽  
Chrysanthos Petropoulos ◽  
Eleni Jelastopulu

2006 ◽  
Vol 47 (11) ◽  
pp. 2475-2481 ◽  
Author(s):  
Erdembileg Anuurad ◽  
Jill Rubin ◽  
Guijing Lu ◽  
Thomas A. Pearson ◽  
Steve Holleran ◽  
...  

Obesity ◽  
2013 ◽  
Vol 21 (3) ◽  
pp. E314-E321 ◽  
Author(s):  
Aris Bechlioulis ◽  
Konstantinos Vakalis ◽  
Katerina K. Naka ◽  
Christos V. Bourantas ◽  
Nikolaos D. Papamichael ◽  
...  

2021 ◽  
Author(s):  
Lima Hazarika ◽  
Supriyo Sen ◽  
Akshaykumar Zawar ◽  
Jitesh Doshi

AbstractA significant genetic suspect for coronary artery disease is the pathological adaptation of apolipoprotein E4 (APOE4) through intramolecular interaction. With the prevailing evidences on APOE4 genotype and its prevalence in coronary artery disease, the present study has investigated the protein–ligand binding affinity and unveil the receptor binding abilities of different classes of ligands for APOE4 through molecular docking studies. Structural basis of APOE4 involvement in CAD suggests that the intramolecular domain interactions to be a suitable target for therapeutic intervention. Various classes of ligands including known drugs used in the treatment of CAD, fragment-based stabilizers and their similar structures and molecules with known bioactivity against APOE4 were screened for their binding affinity and further investigated for their interactions with APOE4. Computational studies show the benzyl amide derived structures to be useful candidates in modulation of APOE4. The dynamics of the binding analysis can be further achieved with an in-depth understanding of drug-receptor interactions performing molecular dynamic simulation studies.


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Qingyuan Zhao ◽  
Jingshu Wang ◽  
Zhen Miao ◽  
Nancy R Zhang ◽  
Sean Hennessy ◽  
...  

Recent genetic data can offer important insights into the roles of lipoprotein subfractions and particle sizes in preventing coronary artery disease (CAD), as previous observational studies have often reported conflicting results. We used the LD score regression to estimate the genetic correlation of 77 subfraction traits with traditional lipid profile and identified 27 traits that may represent distinct genetic mechanisms. We then used Mendelian randomization (MR) to estimate the causal effect of these traits on the risk of CAD. In univariable MR, the concentration and content of medium high-density lipoprotein (HDL) particles showed a protective effect against CAD. The effect was not attenuated in multivariable analyses. Multivariable MR analyses also found that small HDL particles and smaller mean HDL particle diameter may have a protective effect. We identified four genetic markers for HDL particle size and CAD. Further investigations are needed to fully understand the role of HDL particle size.


2018 ◽  
Vol 118 (06) ◽  
pp. 1088-1100 ◽  
Author(s):  
Joana Batuca ◽  
Marta Amaral ◽  
Catarina Favas ◽  
Gonçalo Justino ◽  
Ana Papoila ◽  
...  

AbstractQuantitative and qualitative defects of high-density lipoprotein (HDL) are important in atherogenesis. In this study, we investigated whether antibodies against HDL components had additional value to conventional cardiovascular risk factors for the diagnosis of ischaemic stroke (IS) and coronary artery disease (CAD). Cross-sectional study was conducted on 53 patients with IS, 51 with CAD and 55 healthy controls, and in vitro studies to validate findings of the clinical study. We determined serum immunoglobulin G (IgG) antibodies against HDL (aHDL), apolipoproteins (aApoA-I, aApoA-II and aApoC-I) and paraoxonase-1 (aPON1) as well as PON1 activity (PON1a), total antioxidant capacity and biomarkers of endothelial activation (serum nitric oxide metabolites, 3-nitrotyrosine, VCAM-1 and ICAM-1); in vitro assays tested the capacity of IgG aHDL purified from high titer patients to inhibit PON1a and to reverse protective effect of HDL on endothelial cells. IgG aHDL, aApoA-I and aPON1 were higher in IS and CAD than controls (p < 0.001), predicted negatively PON1a and positively VCAM-1 and ICAM-1. By adding IgG aHDL and aApoA-I to a traditional cardiovascular risk factors model for IS and by adding IgG aHDL in a similar model for CAD, we obtained better discrimination of IS and CAD from healthy controls. IgG aHDL purified from IS and CAD inhibited PON1a by 38% (p < 0.01) and abrogated the protective effect of HDL on VCAM-1 expression by 126% compared with non-specific human IgG (p < 0.001). IgG against HDL components interfere with the antioxidant and anti-inflammatory properties of HDL and may represent novel biomarkers for vascular disease that need to be investigated in prospective studies.


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