Xanthine oxidoreductase polymorphisms: influence in blood pressure and oxidative stress levels

Chaves, Felipe Javier; Corella, Dolores; Blesa, Sebastian; Mansego, María L.; Marín, Pilar; Portolés, Olga; Sorlí, José V.; González-Albert,; Mc, Tormos; Ab, García-García; Sáez, Guillermo T.; Redón, Josep

doi:10.1097/01.fpc.0000239970.23723.38

Cited by 28 publications

(25 citation statements)

References 40 publications

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“…If true, this might also explain the lack of association, as a polymorphism that would increase serum levels would paradoxically reduce intracellular levels. Indeed, there is evidence that polymorphisms of XOR associated with increased activity are associated with hypertension [104,105].…”

Section: Limitations and Controversiesmentioning

confidence: 99%

Uric Acid and Hypertension: Cause or Effect?

et al. 2010

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Uric acid was first associated with primary hypertension in 1874, yet its role in this condition remains unclear. Historically, uric acid was thought to be a secondary response to hypertension or its associated conditions. However, more recent experimental and clinical studies suggest that uric acid could have a contributory role in the pathogenesis of elevated blood pressure. More studies are needed to help dissect the potential mechanisms by which uric acid could initiate this response. It remains possible that uric acid is a marker for xanthine oxidase-associated oxidants and that the latter could be driving the hypertensive response. However, the weight of the evidence suggests that uric acid is a true modifying and possibly causal factor for human primary hypertension. Hence, early management of hyperuricemia might delay the development of essential hypertension.

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Section: Limitations and Controversiesmentioning

confidence: 99%

Uric Acid and Hypertension: Cause or Effect?

et al. 2010

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“…At the population level, several polymorphisms of genes implicated in red-ox balance have been proposed as implicated in hypertension development with contrasting results [25][26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Vanin-1 T26I polymorphism, hypertension and cardiovascular events in two large urban-based prospective studies in Swedes

Fava

Montagnana

Danese

et al. 2013

Nutrition, Metabolism and Cardiovascular Diseases

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Vanin-1 T26I polymorphism, hypertension and cardiovascular events in two large urban-based prospective studies in Swedes.Fava, Cristiano; Montagnana, Martina; Danese, E; Sjögren, Marketa; Almgren, Peter; Engström, Gunnar; Hedblad, Bo; Guidi, G C; Minuz, P; Melander, Olle Link to publication Citation for published version (APA): Fava, C., Montagnana, M., Danese, E., Sjögren, M., Almgren, P., Engström, G., ... Melander, O. (2011). Vanin-1 T26I polymorphism, hypertension and cardiovascular events in two large urban-based prospective studies in Swedes. Nutrition Metabolism and Cardiovascular Diseases. DOI: 10.1016DOI: 10. /j.numecd.2011 General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal ABSTRACT Background: Vanin-1 (gene name VNN1) is an enzyme with pantetheinase activity generating the amino-thiol cysteamine which is implicated in the regulation of redox status through its effect on glutathione. We tested the hypothesis that the rs2294757 VNN1 T26I polymorphism could affect blood pressure (BP) levels, hypertension prevalence, and risk of incident cardiovascular events. Methods:The VNN1 T26I polymorphism was genotyped in 5664 participants of the cardiovascular cohort of the "Malmö Diet and Cancer" (MDC-CVA) study and successively in 17874 participants of the "Malmö Preventive project"(MPP). The incidence of cardiovascular events was monitored for an average of nearly 12 years of follow-up in the MDC-CVA and for 25 years in the MPP.Results: Both before and after adjustment for sex, age and BMI in the MDC-CVA the polymorphism had a mild lowering effect on diastolic BP and hypertension, especially in females.However in MPP no effect on BP phenotypes was detectable. Before and after adjustment for major cardiovascular risk factors, the hazard ratio for incident ischemic stroke and coronary events in MDC-CVA was not significantly different in carriers of different genotypes. Conclusions:Our data do not support a major role for the VNN1 T26I variant in determining BP level and incident ischemic events.

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“…Common genetic polymorphisms within the promoter and exon sequences of CYBA, the gene that encodes the p22(phox) subunit of NADPH oxidase, have been characterized in the context of cardiovascular diseases [18]. Likewise, polymorphisms and haplotypes of the xanthine-oxidase gene have also been linked with higher oxidative stress and BP levels in two different populations [15]. Moreover, the possible influence of common genetic variants of genes codifying for the main antioxidant enzymes has been previously explored in a few studies with discordant results.…”

Section: Introductionmentioning

confidence: 98%

“…In HTN, which has been considered a model of chronic oxidative stress, excessive ROS results from an increase in the activity of pro-oxidant enzymes, mainly NADPH oxidase [13,14] and xanthine-oxidase [15], and from an inadequate response of the main cytoplasmatic antioxidant systems [16,17].…”

Section: Introductionmentioning

confidence: 99%