{'fraction_non_alphanumeric': 0.029532967032967032, 'fraction_numerical': 0.023351648351648352, 'mean_word_length': 5.096234309623431, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Common single nucleotide polymorphisms of the p22phox NADPH oxidase subunit do not influence aortic stiffness in young, healthy adults.

INTRODUCTION
Aortic stiffness is a valuable biomarker for stratifying cardiovascular risk. NADPH oxidase regulates oxidative status in vessels; its single nucleotide polymorphisms (SNPs) modify the redox state of carriers and may lead to noxious structural alterations and affect the vasomotor properties of arteries. We hypothesized that genetic variability of NADPH oxidase would be accompanied by differences in aortic stiffness; to this end, we explored the interplay of pulse wave velocity (PWV), a measure of aortic stiffness, with common SNPs of the CYBA gene that encodes the p22phox subunit of NADPH oxidase.


METHODS
289 young, healthy adults were studied. The -930A/G, A640G and C242T CYBA SNPs were genotyped and PWV was measured. Differences in PWV across genotypes were examined in unadjusted models and after adjustment for confounders.


RESULTS
Genetic variability of the examined SNPs did not result in changes of aortic stiffness. In unadjusted models, PWV did not differ across genotypes for the -930A/G (p=0.20), A640G (p=0.65) or C242T SNP (p=0.50). In stepwise multiple linear regression analysis only sex, age and systolic blood pressure emerged as independent predictors of PWV.


CONCLUSIONS
Common genetic variants of NADPH oxidase do not influence aortic stiffness in young, healthy adults.