scholarly journals Association of genetic polymorphisms in the Matrix Gla Protein (MGP) gene with coronary artery disease and serum mgp levels

2019 ◽  
Vol 22 (2) ◽  
pp. 43-50
Author(s):  
S Karsli-Ceppioglu ◽  
S Yazar ◽  
Y Keskin ◽  
M Karaca ◽  
NE Luleci ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Gene Polymorphisms ◽  
Regulatory Protein ◽  
Matrix Gla Protein ◽  
Arterial Calcification ◽  
Coronary Artery Diseases ◽  
Related Gene ◽  
The Matrix ◽  
Artery Disease

AbstractMatrix Gla protein (MGP) is an important regulatory protein for inhibition of calcification in the vessel wall and cartilage. The MGP gene polymorphisms are suspected to increase the risk of extracellular calcification through altering the related gene expression and serum MGP levels. The goal of this study was to examine the correlation between rs4236 (Thr83-Ala), rs12304 (Glu60-X) and rs1800802 (T138-C) polymorphisms of the MGP gene and coronary artery calcification. Serum MGP levels of 168 subjects who had undergone coronary angiography were analyzed along with genotyping of MGP gene polymorphisms. The results indicated that serum MGP levels were significantly associated with rs4236 and rs1800802 polymorphisms of the MGP gene with the occurrence of coronary artery diseases (CAD). Allelic distributions of MGP gene polymorphisms and serum MGP levels, respectively, were not significantly interconnected with the presence of CAD. Our results revealed that serum MGP levels of CAD patients show association with rs4236 and rs1800802 polymorphisms, but serum MGP levels alone do not directly reflect the risk of CAD. The role of MGP genetic variants on formation and progression of arterial calcification should be regarded in cardiovascular diseases.

scholarly journals Role of Matrix Gla Protein in the Complex Network of Coronary Artery Disease: A Comprehensive Review

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 737
Author(s):  
Marko Kumric ◽  
Josip A. Borovac ◽  
Tina Ticinovic Kurir ◽  
Dinko Martinovic ◽  
Ivan Frka Separovic ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Complex Network ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Clinical Decision Making ◽  
Large Body ◽  
Matrix Gla Protein ◽  
Artery Disease

Coronary artery disease (CAD) is widely recognized as one of the most important clinical entities. In recent years, a large body of accumulated data suggest that coronary artery calcification, a process highly prevalent in patients with CAD, occurs via well-organized biologic processes, rather than passively, as previously regarded. Matrix Gla protein (MGP), a vitamin K-dependent protein, emerged as an important inhibitor of both intimal and medial vascular calcification. The functionality of MGP hinges on two post-translational modifications: phosphorylation and carboxylation. Depending on the above-noted modifications, various species of MGP may exist in circulation, each with their respective level of functionality. Emerging data suggest that dysfunctional species of MGP, markedly, dephosphorylated-uncarboxylated MGP, might find its application as biomarkers of microvascular health, and assist in clinical decision making with regard to initiation of vitamin K supplementation. Hence, in this review we summarized the current knowledge with respect to the role of MGP in the complex network of vascular calcification with concurrent inferences to CAD. In addition, we discussed the effects of warfarin use on MGP functionality, with concomitant implications to coronary plaque stability.

scholarly journals Association of genetic polymorphisms in SOD2, SOD3, GPX3, and GSTT1 with hypertriglyceridemia and low HDL-C level in subjects with high risk of coronary artery disease

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7407
Author(s):  
Nisa Decharatchakul ◽  
Chatri Settasatian ◽  
Nongnuch Settasatian ◽  
Nantarat Komanasin ◽  
Upa Kukongviriyapan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
High Risk ◽  
Gene Polymorphisms ◽  
Coronary Atherosclerosis ◽  
Atherogenic Dyslipidemia ◽  
Related Gene ◽  
Low Hdl ◽  
Artery Disease

Background Oxidative stress modulates insulin resistant-related atherogenic dyslipidemia: hypertriglyceridemia (HTG) and low high-density lipoprotein cholesterol (HDL-C) level. Gene polymorphisms in superoxide dismutase (SOD2 and SOD3), glutathione peroxidase-3 (GPX3), and glutathione S-transferase theta-1 (GSTT1) may enable oxidative stress-related lipid abnormalities and severity of coronary atherosclerosis. The present study investigated the associations of antioxidant-related gene polymorphisms with atherogenic dyslipidemia and atherosclerotic severity in subjects with high risk of coronary artery disease (CAD). Methods Study population comprises of 396 subjects with high risk of CAD. Gene polymorphisms: SOD2 rs4880, SOD3 rs2536512 and rs2855262, GPX rs3828599, and GSTT1 (deletion) were evaluated the associations with HTG, low HDL-C, high TG/HDL-C ratio, and severity of coronary atherosclerosis. Results SOD2 rs4880-CC, SOD3 rs2536512-AA, rs2855262-CC, and GPX3 rs3828599-AA, but not GSTT1-/- individually increased risk of HTG combined with low HDL-C level. With a combination of five risk-genotypes as a genetic risk score (GRS), GRS ≥ 6 increased risks of low HDL-C, high TG/HDL-C ratio, and HTG combined with low HDL-C, comparing with GRS 0–2 [respective adjusted ORs (95% CI) = 2.70 (1.24–5.85), 3.11 (1.55–6.23), and 5.73 (2.22–14.77)]. Gene polymorphisms, though, were not directly associated with severity of coronary atherosclerosis; high TG/HDL-C ratio was associated with coronary atherosclerotic severity [OR = 2.26 (95% CI [1.17–4.34])]. Conclusion Combined polymorphisms in antioxidant-related genes increased the risk of dyslipidemia related to atherosclerotic severity, suggesting the combined antioxidant-related gene polymorphisms as predictor of atherogenic dyslipidemia.

scholarly journals THE ROLE OF GENE POLYMORPHISMS IN INDIVIDUALLY CHANGING OF THE LIPID PROFILE AMONG PATIENTS WITH CORONARY ARTERY DISEASE UNDER THE INFLUENCE OF THE STATIN THERAPY

2019 ◽  
Vol 42 (3) ◽  
pp. 72-77
Author(s):  
Fushtey I. M. ◽  
Sid E. V ◽  
Litvinenko V. V.
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Lipid Metabolism ◽  
Coronary Artery ◽  
Statin Therapy ◽  
Gene Polymorphisms ◽  
Artery Disease ◽  
Protein Transporters

Ischemic heart disease is one of the urgent problems in modern cardiology, which is associated with a wide spread of disability and mortality mainly among young and employable aged people. The therapeutic drugs effect is individual and depends on the genetic characteristics of the patient. The aim of the study. Analysis of modern literature sources related to the role of gene polymorphisms in individual lipid profile changing among patients with coronary artery disease under the influence of the statin therapy. Literature review. Pharmacotherapy while ischemic heart disease (IHD) provides for mandatory preventive services aimed at the eliminating of modifying risk factors of coronary heart disease. One of the most important indicators of successful treatment of patients with IHD is a lipid metabolism state, that is why treatment can’t be imagined without the inclusion of statins in therapeutic schemes of dyslipidemia correction. The current understanding of the statins effectiveness is based on the knowledge of molecular mechanisms underlying the pharmacokinetics and pharmacodynamics processes. In clinical practice, while taking statins with absolute compliance of patients and elimination of all modifying factors, lipid metabolism parameters are not always normalized, this indicates characteristics of the patients’ genetic. Of particular importance is the effect of genotype on pharmacotherapy using protein transporters, carriers of endogenous compounds or xenobiotics through biological membranes assisted by passive or active mechanisms. Single-nucleotide polymorphisms (SNPs) of transport proteins can change the absorption and excretion degree of drugs and their metabolites. Polypeptides of organic anions membrane transporters that regulate cell uptake of certain endogenous substances and drugs are encoded by SLCO genes. One of the main absorption protein transporters is OATP1B1. It is established that the effects of some SLCO1B1 SNPs on transport function are substrate dependent, and the most studied among them are с.521Т>С and с.388А>G. The c.521Т>C and с.388А>G polymorohisms c.521T>C". Но c.521T>C are in an intermittent contact with each other, and despite this they exist in a variety of SLCO1B1-haplotypes. The c.388А-521Т haplotypes known as *1A ones, c.388G-521Т as *1B, c. 388А-521С as *5 and c.388G-521С as *15. One of the first studies showed that *5 and *15 haplotypes were associated with a decrease in the absorption of statins. In further studies of c.521C allele it was found a related increase of the statins concentration in human plasma, which leads to the progression of undesirable reactions such as myalgia, myopathy, and even rhabdomyolysis, asymptomatic increase transaminase activity and abdominal pain. The study of SLCO1B1 pharmacogenetics found that dysfunction of the protein-transporter leads to reduced absorption by the liver cells, the increasing of plasma concentrations and the change in the body's response to stationery. Conclusion. Analysis of the literature indicates that the therapeutic effect of statins in combination with genetic polymorphisms may have an individual effect on the pharmacokinetics of these drugs. To study the influence of SLCO1B1 c.521Т>С gene polymorphism there are needed the further researches in populations with IHD. A more detailed study of this polymorphism from the perspective of personalized therapy will allow developing individual approaches to the appointment of statins. Keywords: coronary heart disease, statin therapy, gene polymorphism, transporter proteins, personalized therapy.

Mo-P2:195 Role of hemostatic gene polymorphisms in the early development of coronary artery disease

2006 ◽  
Vol 7 (3) ◽  
pp. 89
Author(s):  
E.Y. Andreenko ◽  
A.N. Meshkov ◽  
A.V. Balatsky ◽  
P.I. Makarevich ◽  
M.R. Lalayane ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Early Development ◽  
Gene Polymorphisms ◽  
Artery Disease

scholarly journals Coronary Artery Disease: A Study on the Joint Role of Birth Weight, Adenosine Deaminase, and Gender

2009 ◽  
Vol 2009 ◽  
pp. 1-6
Author(s):  
F. Gloria-Bottini ◽  
M. Banci ◽  
P. Saccucci ◽  
N. Lucarini ◽  
F. Ianniello ◽  
...  
Keyword(s):  
Birth Weight ◽  
Coronary Artery ◽  
Adenosine Deaminase ◽  
Dna Analysis ◽  
Adult Life ◽  
Ratio Analysis ◽  
Coronary Artery Diseases ◽  
Artery Disease ◽  
And Gender

An inverse relationship between birth weight and coronary artery diseases is well documented but it remains unclear which exposure in early life might underlie such association. Recently it has been reported an association between adenosine deaminase genetic polymorphism and coronary artery diseases. Gender differences in the degree of this association have been also observed. These observations prompted us to study the possible joint effects of BW, ADA, and gender on the susceptibility to coronary artery diseases. 222 subjects admitted to hospital for nonfatal coronary artery diseases, and 762 healthy consecutive newborns were studied. ADA genotypes were determined by DNA analysis. A highly significant complex relationship has emerged among ADA, birth weight, and gender concerning their role on susceptibility to coronary artery diseases in adult life. Odds ratio analysis suggests that low birth weight is more important in females than in males. ADA∗2 allele appears protective in males, while in females such effect is obscured by birth weight.

scholarly journals Role of interleukin-6 gene polymorphisms in the risk of coronary artery disease

2015 ◽  
Vol 14 (2) ◽  
pp. 3177-3183 ◽  
Author(s):  
K. Wang ◽  
P.S. Dong ◽  
H.F. Zhang ◽  
Z.J. Li ◽  
X.M. Yang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Interleukin 6 ◽  
Gene Polymorphisms ◽  
Artery Disease
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