Association between a gene variant near ataxia telangiectasia mutated and coronary artery disease in men

8Citations
Citations of this article
35Readers
Mendeley users who have this article in their library.

Abstract

Objective: Type 2 diabetes is accompanied by increased mortality from coronary artery disease (CAD), but the mechanisms linking these conditions remain elusive. Hence, treatment of hyperglycaemia alone is not sufficient to avoid CAD in diabetes. Alternative views suggest that metabolic and vascular diseases share unifying cellular defects that could serve as targets for novel therapeutic strategies. Recently, a variant [single-nucleotide polymorphism (SNP); rs11212617] near the gene for ataxia telangiectasia mutated (ATM) has been associated with glycaemic response to metformin. Materials and methods: We determined rs11212617 in 240 male patients who underwent elective coronary angiography. Results: While the variant was not associated with glucose concentrations, the A allele was significantly associated with the presence of CAD (chi-square, p = 0.003), as well as with logarithmically transformed quantitative CAD indices [severe score (SS): 0.5 (0.4-0.6) vs 0.3 (0.2-0.5); extent score (ES): 2.63 (2.4-2.9) vs 1.94 (1.4-2.4), both p < 0.05, respectively]. Multivariate analysis revealed an independent association between the A allele with ES (β = 0.17, p < 0.01). Conclusion: Our data suggest that ATM-dependent signalling might play a role in the development of atherosclerotic vascular disease, but larger studies are necessary to substantiate such a hypothesis. © The Author(s) 2013.

Cite

CITATION STYLE

APA

Schiekofer, S., Bobak, I., Kleber, M. E., Maerz, W., Rudofsky, G., Dugi, K. A., & Schneider, J. G. (2014). Association between a gene variant near ataxia telangiectasia mutated and coronary artery disease in men. Diabetes and Vascular Disease Research, 11(1), 60–63. https://doi.org/10.1177/1479164113514232

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free