Relevant bibliographies by topics / Atherogenesis; Gene encoding

Contents

  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Atherogenesis; Gene encoding'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Atherogenesis; Gene encoding.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Atherogenesis; Gene encoding"

1

Lozhkin, A. P., T. B. Biktagirov, O. V. Gorshkiv, E. V. Timonina, G. V. Mamin, S. B. Orlinskii, N. I. Silkin, et al. "Manganese in atherogenesis: detection, origin, and role." Biomeditsinskaya Khimiya 58, no. 3 (2012): 291–99. http://dx.doi.org/10.18097/pbmc20125803291.

Full text
Abstract:
The role of transition metal ions in atherogenesis is controversial; they can participate in the hydroxyl radical generation and catalyze the reactive oxygen species neutralization reaction as cofactors of antioxidant enzymes. Using EPR spectroscopy, we revealed that 70% of the samples of aorta with atherosclerotic lesions possessed superoxide dismutase activity, 100% of the samples initiated Fenton reaction and demonstrated the presence of manganese paramagnetic centers. The sodA gene encoding manganese-dependent bacterial superoxide dismutase was not found in the samples of atherosclerotic plaques by PCR using degenerate primers. The data obtained indicates the perspectives of manganese analysis as a marker element in the express diagnostics of atherosclerosis.
APA, Harvard, Vancouver, ISO, and other styles
2

Ponomarenko, Mikhail, Dmitry Rasskazov, Irina Chadaeva, Ekaterina Sharypova, Irina Drachkova, Dmitry Oshchepkov, Petr Ponomarenko, et al. "Candidate SNP Markers of Atherogenesis Significantly Shifting the Affinity of TATA-Binding Protein for Human Gene Promoters Show Stabilizing Natural Selection as a Sum of Neutral Drift Accelerating Atherogenesis and Directional Natural Selection Slowing It." International Journal of Molecular Sciences 21, no. 3 (February 5, 2020): 1045. http://dx.doi.org/10.3390/ijms21031045.

Full text
Abstract:
(1) Background: The World Health Organization (WHO) regards atherosclerosis-related myocardial infarction and stroke as the main causes of death in humans. Susceptibility to atherogenesis-associated diseases is caused by single-nucleotide polymorphisms (SNPs). (2) Methods: Using our previously developed public web-service SNP_TATA_Comparator, we estimated statistical significance of the SNP-caused alterations in TATA-binding protein (TBP) binding affinity for 70 bp proximal promoter regions of the human genes clinically associated with diseases syntonic or dystonic with atherogenesis. Additionally, we did the same for several genes related to the maintenance of mitochondrial genome integrity, according to present-day active research aimed at retarding atherogenesis. (3) Results: In dbSNP, we found 1186 SNPs altering such affinity to the same extent as clinical SNP markers do (as estimated). Particularly, clinical SNP marker rs2276109 can prevent autoimmune diseases via reduced TBP affinity for the human MMP12 gene promoter and therefore macrophage elastase deficiency, which is a well-known physiological marker of accelerated atherogenesis that could be retarded nutritionally using dairy fermented by lactobacilli. (4) Conclusions: Our results uncovered SNPs near clinical SNP markers as the basis of neutral drift accelerating atherogenesis and SNPs of genes encoding proteins related to mitochondrial genome integrity and microRNA genes associated with instability of the atherosclerotic plaque as a basis of directional natural selection slowing atherogenesis. Their sum may be stabilizing the natural selection that sets the normal level of atherogenesis.
APA, Harvard, Vancouver, ISO, and other styles
3

Xu, Jing, Wenlong Li, Xunna Bao, Hu Ding, Jingzhou Chen, Weili Zhang, Kai Sun, et al. "Association of putative functional variants in the PLAU gene and the PLAUR gene with myocardial infarction." Clinical Science 119, no. 8 (July 6, 2010): 353–59. http://dx.doi.org/10.1042/cs20100151.

Full text
Abstract:
uPA (urokinase-plasminogen activator) and its receptor (uPAR) have been implicated in a broad spectrum of pathophysiological processes, including fibrinolysis, proteolysis, inflammation, atherogenesis and plaque destabilization, all of which are involved in the pathogenesis of MI (myocardial infarction). We hypothesized that putative functional genetic variation in the two genes encoding uPA and uPAR (PLAU and PLAUR respectively) might influence the susceptibility to MI. We genotyped rs4065 [3′-UTR (untranslated region) *141C>T) and rs2227564 (Pro141Leu) in the PLAU gene as well as rs344781 (−516T>C) in the PLAUR gene in 633 MI patients and 1237 gender- and age-matched control subjects. Our results showed that the T allele of rs4065 was significantly associated with an increased risk of MI, with an adjusted OR (odds ratio) of 1.38 [95% CI (confidence interval), 1.07–1.78; P=0.012) under the dominant model, 1.4 (95% CI, 1.12–1.75; P=0.003) under the additive model and 2.5 (95% CI, 1.15–5.41; P=0.02) under the recessive model. The findings were then replicated in another independent case-control study including 545 MI patients and 597 control subjects. In conclusion, our results suggest that rs4065 might be a previously unknown genetic risk factor for MI in the Chinese Han population.
APA, Harvard, Vancouver, ISO, and other styles
4

Galgani, Andrea, AnaMaria Valdes, Henry A. Erlich, Calvin Mano, Suzanne Cheng, Antonio Petrone, Federica Sentinelli, Andrea Berni, Marco G. Baroni, and Raffaella Buzzetti. "Homozygosity for the Ala Allele of the PPARγ2 Pro12Ala Polymorphism Is Associated with Reduced Risk of Coronary Artery Disease." Disease Markers 29, no. 5 (2010): 259–64. http://dx.doi.org/10.1155/2010/501730.

Full text
Abstract:
Several studies suggest that the peroxisome proliferator-activated receptor gamma (PPARγ) is involved in atherogenesis. The Pro12Ala polymorphism in the gene encoding PPARγ (PPARγ2 gene) influences the risk for type 2 diabetes. Two population-based studies have shown that the Ala allele is associated with reduced carotid intimal-medial thickness (IMT). However, studies focusing on acute clinical events have yielded conflicting results. Our aim was to evaluate the role of the Pro12AlaPPARγ2 polymorphism on the risk of coronary artery disease (CAD) in an Italian population with a case-controlled genetic association study in which 478 CAD patients and 218 controls were genotyped for the Pro12Ala polymorphism. CAD was diagnosed by angiography. We found that homozygotes for the Ala12 allele had a significantly reduced risk of CAD after adjusting for diabetes, sex, age, body mass index (BMI), smoking, lipids and hypertension (OR = 0.007; 95% C.I. = 0.00–0.32p< 0.011). In this casecontrol study, homozygosity for the Ala allele at codon 12 of thePPAR2 gene resulted in reduced risk of CAD. This is consistent with reports from previous studies focusing on atherosclerosis and myocardial infarction.
APA, Harvard, Vancouver, ISO, and other styles
5

Gold, Elizabeth S., Stephen A. Ramsey, Mark J. Sartain, Jyrki Selinummi, Irina Podolsky, David J. Rodriguez, Robert L. Moritz, and Alan Aderem. "ATF3 protects against atherosclerosis by suppressing 25-hydroxycholesterol–induced lipid body formation." Journal of Experimental Medicine 209, no. 4 (April 2, 2012): 807–17. http://dx.doi.org/10.1084/jem.20111202.

Full text
Abstract:
Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-loaded macrophages in the arterial wall. We demonstrate that macrophage lipid body formation can be induced by modified lipoproteins or by inflammatory Toll-like receptor agonists. We used an unbiased approach to study the overlap in these pathways to identify regulators that control foam cell formation and atherogenesis. An analysis method integrating epigenomic and transcriptomic datasets with a transcription factor (TF) binding site prediction algorithm suggested that the TF ATF3 may regulate macrophage foam cell formation. Indeed, we found that deletion of this TF results in increased lipid body accumulation, and that ATF3 directly regulates transcription of the gene encoding cholesterol 25-hydroxylase. We further showed that production of 25-hydroxycholesterol (25-HC) promotes macrophage foam cell formation. Finally, deletion of ATF3 in Apoe−/− mice led to in vivo increases in foam cell formation, aortic 25-HC levels, and disease progression. These results define a previously unknown role for ATF3 in controlling macrophage lipid metabolism and demonstrate that ATF3 is a key intersection point for lipid metabolic and inflammatory pathways in these cells.
APA, Harvard, Vancouver, ISO, and other styles
6

Weber, Kim S. C., Georg Draude, Wolfgang Erl, Rainer de Martin, and Christian Weber. "Monocyte Arrest and Transmigration on Inflamed Endothelium in Shear Flow Is Inhibited by Adenovirus-Mediated Gene Transfer of IκB-." Blood 93, no. 11 (June 1, 1999): 3685–93. http://dx.doi.org/10.1182/blood.v93.11.3685.

Full text
Abstract:
Abstract Mobilization of nuclear factor-κB (NF-κB) activates transcription of genes encoding endothelial adhesion molecules and chemokines that contribute to monocyte infiltration critical in atherogenesis. Inhibition of NF-κB has been achieved by pharmacological and genetic approaches; however, monocyte interactions with activated endothelium in shear flow following gene transfer of the NF-κB inhibitor IκB- have not been studied. We found that overexpression of IκB- in endothelial cells using a recombinant adenovirus prevented tumor necrosis factor- (TNF-)–induced degradation of IκB- and suppressed the upregulation of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin mRNA and surface protein expression and the upregulation of transcripts for the chemokines monocyte chemoattractant protein 1 (MCP-1) and growth-related activity- (GRO-) by TNF-. This was associated with a reduction in endothelial MCP-1 secretion and GRO- immobilization. Adhesion assays under physiological shear flow conditions showed that firm arrest, spreading, and transmigration of monocytes on TNF-–activated endothelium was markedly inhibited by IκB- overexpression. Inhibition with monoclonal antibodies and peptide antagonists inferred that this was due to reduced expression of Ig integrin ligand as well as of chemokines specifically involved in these events. In contrast, rolling of monocytes was increased by IκB- transfer and was partly mediated by P-selectin; however, it appeared to be unaffected by the inhibition of E-selectin induction. Thus, our data provide novel evidence that selective modulation of NF-κB by adenoviral transfer of IκB- impairs the expression of multiple endothelial gene products required for subsequent monocyte arrest and emigration in shear flow and thus for monocyte infiltration in atherosclerotic plaques.
APA, Harvard, Vancouver, ISO, and other styles
7

Weber, Kim S. C., Georg Draude, Wolfgang Erl, Rainer de Martin, and Christian Weber. "Monocyte Arrest and Transmigration on Inflamed Endothelium in Shear Flow Is Inhibited by Adenovirus-Mediated Gene Transfer of IκB-." Blood 93, no. 11 (June 1, 1999): 3685–93. http://dx.doi.org/10.1182/blood.v93.11.3685.411k16_3685_3693.

Full text
Abstract:
Mobilization of nuclear factor-κB (NF-κB) activates transcription of genes encoding endothelial adhesion molecules and chemokines that contribute to monocyte infiltration critical in atherogenesis. Inhibition of NF-κB has been achieved by pharmacological and genetic approaches; however, monocyte interactions with activated endothelium in shear flow following gene transfer of the NF-κB inhibitor IκB- have not been studied. We found that overexpression of IκB- in endothelial cells using a recombinant adenovirus prevented tumor necrosis factor- (TNF-)–induced degradation of IκB- and suppressed the upregulation of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin mRNA and surface protein expression and the upregulation of transcripts for the chemokines monocyte chemoattractant protein 1 (MCP-1) and growth-related activity- (GRO-) by TNF-. This was associated with a reduction in endothelial MCP-1 secretion and GRO- immobilization. Adhesion assays under physiological shear flow conditions showed that firm arrest, spreading, and transmigration of monocytes on TNF-–activated endothelium was markedly inhibited by IκB- overexpression. Inhibition with monoclonal antibodies and peptide antagonists inferred that this was due to reduced expression of Ig integrin ligand as well as of chemokines specifically involved in these events. In contrast, rolling of monocytes was increased by IκB- transfer and was partly mediated by P-selectin; however, it appeared to be unaffected by the inhibition of E-selectin induction. Thus, our data provide novel evidence that selective modulation of NF-κB by adenoviral transfer of IκB- impairs the expression of multiple endothelial gene products required for subsequent monocyte arrest and emigration in shear flow and thus for monocyte infiltration in atherosclerotic plaques.
APA, Harvard, Vancouver, ISO, and other styles
8

Price, Nathan L., Xinbo Zhang, Pablo Fernández-Tussy, Abhishek K. Singh, Sean A. Burnap, Noemi Rotllan, Leigh Goedeke, et al. "Loss of hepatic miR-33 improves metabolic homeostasis and liver function without altering body weight or atherosclerosis." Proceedings of the National Academy of Sciences 118, no. 5 (January 25, 2021): e2006478118. http://dx.doi.org/10.1073/pnas.2006478118.

Full text
Abstract:
miR-33 is an intronic microRNA within the gene encoding the SREBP2 transcription factor. Like its host gene, miR-33 has been shown to be an important regulator of lipid metabolism. Inhibition of miR-33 has been shown to promote cholesterol efflux in macrophages by targeting the cholesterol transporter ABCA1, thus reducing atherosclerotic plaque burden. Inhibition of miR-33 has also been shown to improve high-density lipoprotein (HDL) biogenesis in the liver and increase circulating HDL-C levels in both rodents and nonhuman primates. However, evaluating the extent to which these changes in HDL metabolism contribute to atherogenesis has been hindered by the obesity and metabolic dysfunction observed in whole-body miR-33–knockout mice. To determine the impact of hepatic miR-33 deficiency on obesity, metabolic function, and atherosclerosis, we have generated a conditional knockout mouse model that lacks miR-33 only in the liver. Characterization of this model demonstrates that loss of miR-33 in the liver does not lead to increased body weight or adiposity. Hepatic miR-33 deficiency actually improves regulation of glucose homeostasis and impedes the development of fibrosis and inflammation. We further demonstrate that hepatic miR-33 deficiency increases circulating HDL-C levels and reverse cholesterol transport capacity in mice fed a chow diet, but these changes are not sufficient to reduce atherosclerotic plaque size under hyperlipidemic conditions. By elucidating the role of miR-33 in the liver and the impact of hepatic miR-33 deficiency on obesity and atherosclerosis, this work will help inform ongoing efforts to develop novel targeted therapies against cardiometabolic diseases.
APA, Harvard, Vancouver, ISO, and other styles
9

Salerno, Alessandro G., Thiago Rentz, Gabriel G. Dorighello, Ana Carolina Marques, Estela Lorza-Gil, Amarylis C. B. A. Wanschel, Audrey de Moraes, Anibal E. Vercesi, and Helena C. F. Oliveira. "Lack of mitochondrial NADP(H)-transhydrogenase expression in macrophages exacerbates atherosclerosis in hypercholesterolemic mice." Biochemical Journal 476, no. 24 (December 20, 2019): 3769–89. http://dx.doi.org/10.1042/bcj20190543.

Full text
Abstract:
The atherosclerosis prone LDL receptor knockout mice (Ldlr−/−, C57BL/6J background) carry a deletion of the NADP(H)-transhydrogenase gene (Nnt) encoding the mitochondrial enzyme that catalyzes NADPH synthesis. Here we hypothesize that both increased NADPH consumption (due to increased steroidogenesis) and decreased NADPH generation (due to Nnt deficiency) in Ldlr−/− mice contribute to establish a macrophage oxidative stress and increase atherosclerosis development. Thus, we compared peritoneal macrophages and liver mitochondria from three C57BL/6J mice lines: Ldlr and Nnt double mutant, single Nnt mutant and wild-type. We found increased oxidants production in both mitochondria and macrophages according to a gradient: double mutant &gt; single mutant &gt; wild-type. We also observed a parallel up-regulation of mitochondrial biogenesis (PGC1a, TFAM and respiratory complexes levels) and inflammatory (iNOS, IL6 and IL1b) markers in single and double mutant macrophages. When exposed to modified LDL, the single and double mutant cells exhibited significant increases in lipid accumulation leading to foam cell formation, the hallmark of atherosclerosis. Nnt deficiency cells showed up-regulation of CD36 and down-regulation of ABCA1 transporters what may explain lipid accumulation in macrophages. Finally, Nnt wild-type bone marrow transplantation into LDLr−/− mice resulted in reduced diet-induced atherosclerosis. Therefore, Nnt plays a critical role in the maintenance of macrophage redox, inflammatory and cholesterol homeostasis, which is relevant for delaying the atherogenesis process.
APA, Harvard, Vancouver, ISO, and other styles
10

Kanters, Edwin, Marion J. J. Gijbels, Ingeborg van der Made, Monique N. Vergouwe, Peter Heeringa, Georg Kraal, Marten H. Hofker, and Menno P. J. de Winther. "Hematopoietic NF-κB1 deficiency results in small atherosclerotic lesions with an inflammatory phenotype." Blood 103, no. 3 (February 1, 2004): 934–40. http://dx.doi.org/10.1182/blood-2003-05-1450.

Full text
Abstract:
AbstractAtherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden macrophages in the vessel wall. One of the major transcription factors in inflammation is nuclear factor κB (NF-κB), and we have studied its role in the development of atherosclerosis. Bone marrow from mice targeted in the NF-κB1 gene encoding for the p50 subunit was used to reconstitute irradiated LDLR-/- mice as a model for atherosclerosis. After feeding the mice a high-fat diet, those deficient in NF-κB1 had a 41% lower rate of atherosclerosis than control mice, as judged by the sizes of the lesions. Furthermore, in the absence of NF-κB1, the lesions were characterized by an inflammatory phenotype, contained increased numbers of small cells, and were almost devoid of normal foam cells. In vitro studies using bone marrow (BM)-derived macrophages showed that macrophages lacking p50 had a prolonged production of tumor necrosis factor (TNF) in response to lipopolysaccharide (LPS), and other cytokines were also affected. Interestingly, the uptake of oxidized low-density lipoprotein (LDL) was greatly reduced in activated p50-deficient macrophages, probably because of a reduction in the expression of scavenger receptor class A. The effects on atherosclerosis might have resulted from the changes in cytokine production and the uptake of modified lipoproteins, making p50 a pivotal regulator of atherogenesis. (Blood. 2004;103:934-940)
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Atherogenesis; Gene encoding"

1

Zhang, Baiping. "Study of the regulation of expression and activity of gelatinase B in relation to the development of atherosclerosis." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342587.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Atherogenesis; Gene encoding' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography