The contribution of NOS3 variants to coronary artery disease: A combined genetic epidemiology and computational biochemistry perspective

Teralı, Kerem; Ergören, Mahmut Çerkez

doi:10.1016/j.ijbiomac.2018.11.128

Cited by 7 publications

(6 citation statements)

References 54 publications

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“…Ischemic postconditioning increased the expression of Nrf2, NQO1, and HO-1 and impeded MI-induced oxidative stress ( 38 ). The NOS3 c.894G > T and 27-bp VNTR polymorphisms can be used for CAD screening ( 39 ). In the Women’s Genome Health Study, metabolic-syndrome related genes, such as LEPR, HNF1A, IL6R, and GCKR, were correlated to CRP expression and inflammation ( 40 ).…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis and Autophagy-Related Genes in the Pathogenesis of Ischemic Cardiomyopathy

Zheng

Gao

Zhang

et al. 2022

Front. Cardiovasc. Med.

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BackgroundObesity plays an important role in type 2 diabetes mellitus (T2DM) and myocardial infarction (MI). Ferroptosis and ferritinophagy are related to metabolic pathways, such as fatty acid metabolism and mitochondrial respiration. We aimed to investigate the ferroptosis- and autophagy-related differentially expressed genes (DEGs) that might be potential targets for MI progression.MethodsGSE116250 was analyzed to obtain DEGs. A Venn diagram was used to obtain the overlapping ferroptosis- and autophagy-related DEGs. The enrichment pathway analysis was performed and the hub genes were obtained. Pivotal miRNAs, transcription factors, and drugs with the hub genes interactions were also predicted. The MI mice model was constructed, and qPCR analysis and single-cell sequencing were used to validate the hub genes.ResultsUtilizing the limma package and the Venn diagram, 26 ferroptosis-related and 29 autophagy-related DEGs were obtained. The list of ferroptosis-related DEGs was analyzed, which were involved in the cellular response to a toxic substance, cellular oxidant detoxification, and the IL-17 signaling pathway. The list of autophagy-related DEGs was involved in the regulation of autophagy, the regulation of JAK-STAT signaling pathway, and the regulation of MAPK cascade. In the protein-protein interaction network, the hub DEGs, such as IL-6, PTGS2, JUN, NQO1, NOS3, LEPR, NAMPT, CDKN2A, CDKN1A, and Snai1, were obtained. After validation using qPCR analysis in the MI mice model and single-cell sequencing, the 10 hub genes can be the potential targets for MI deterioration.ConclusionThe screened hub genes, IL-6, PTGS2, JUN, NQO1, NOS3, LEPR, NAMPT, CDKN2A, CDKN1A, and Snai1, may be therapeutic targets for patients with MI and may prevent adverse cardiovascular events.

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Section: Discussionmentioning

confidence: 99%

Ferroptosis and Autophagy-Related Genes in the Pathogenesis of Ischemic Cardiomyopathy

Zheng

Gao

Zhang

et al. 2022

Front. Cardiovasc. Med.

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“…In developed western countries, at least half of all deaths are due to cardiovascular diseases and 3/4 of them are related to atherosclerotic coronary artery disease (CAD). It is one of the leading causes of morbidity and mortality [16]. Diabetes mellitus is defined as a complex metabolic syndrome characterized by hyperglycemia, which increases the risk of microvascular and macrovascular disease [1].…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective effects of erythropoietin in diabetic rats determined by CD34 and vascular endothelial growth factor levels

Oztas

Meriç

Beyaz

et al. 2020

Arch Med Sci Atheroscler Dis

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Introduction In this study, the effects of diabetes mellitus on the cardiovascular system were investigated by assessing the stem cell levels in serum and heart and compared with the normal population. Additionally, efficacy of erythropoietin, which is known to increase stem cells, was studied in diabetic rats. Material and methods Twenty-five male Sprague Dawley rats were divided into three groups as a control group (group 1), diabetic group (group 2) and erythropoietin induced diabetic group (group 3). A diabetes model was created with streptozocin. In group 3 rats received 3000 U/kg of erythropoietin. At the end of 1 month blood reticulocyte levels, degree of tissue fibrosis and immunohistochemical assessment of reliable stem cell markers, CD34 and vascular endothelial growth factor (VEGF), were analyzed. Results The increase in the blood glucose levels resulted in a significant decrease in reticulocyte levels in group 2. The increase in blood glucose levels resulted in a statistically significant increase in tissue level of fibrosis, CD34 and VEGF. When the rats in groups 1 and 2 were compared, the fibrosis, CD34 and VEGF levels were found to increase significantly. When group 2 and group 3 were compared, the amount of fibrosis was lower and the levels of CD34 and VEGF were significantly higher in group 3 than group 2. Conclusions The results of our study indicated that the amount of CD34 and VEGF which function in cellular protection and tissue regeneration may be enhanced with safely applicable erythropoietin leading to increase in reticulocyte levels in serum, and CD34 and VEGF levels in right atrium, right ventricle, left atrium, and left ventricle as a protective mechanism in diabetic rats.

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“…Correlation studies showed that this VNTRs is associated with high serum triglyceride levels (versus that of five 27 bp repeats), while the in silico analysis showed that this repeat can affect alternative splicing. 15 Other VNTRs located in myoglobin, interleukin-1 receptor antagonist, DNase 1, and interleukin-4 genes, among others, have been observed to be associated with RA, SLE and osteoarthritis (Table 2). [16][17][18]…”

Section: Figure 2 Image Depicting the Effect Of The Environment; And Of Mutations-polymorphisms In The Genesis Of Mendelian And Multifactmentioning

confidence: 99%

Role of genetic variability in Mendelian and multifactorial diseases

Ramírez‐Bello¹

2023

GMM

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VNTRs and STRs have been used in linkage studies to detect regions involved with Mendelian (or monogenic) diseases, such as Duchenne or Becker muscular dystrophy, cystic fibrosis, sickle cell anemia, etc., which due to their low prevalence are quite rare in populations. These diseases have the characteristic that a single altered gene results in a phenotype (Fig. 1), given that the mutation has great biological effect; however, there are always exceptions and, in some cases, even if a mutation occurs, it will not lead to the disease

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The contribution of NOS3 variants to coronary artery disease: A combined genetic epidemiology and computational biochemistry perspective

Cited by 7 publications

References 54 publications

Ferroptosis and Autophagy-Related Genes in the Pathogenesis of Ischemic Cardiomyopathy

Ferroptosis and Autophagy-Related Genes in the Pathogenesis of Ischemic Cardiomyopathy

Cardioprotective effects of erythropoietin in diabetic rats determined by CD34 and vascular endothelial growth factor levels

Role of genetic variability in Mendelian and multifactorial diseases

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