科研之友
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摘要
Background: Heme-oxygenase 1 (HO-1), an inducible heme-degrading enzyme, has antiatherogenic effects through its enzymatic end products. HO-1 gene expression is modulated by a guanidine thymidine dinucleotide ([GT](n)) repeat polymorphism in the promoter region. Shorter repeats with (GT)(n) < 25 are associated with higher inducibility and activity of HO-1. Methods: We performed a systematic review of all literature from 1997 to 2013 on the association of the HO-1 (GT)(n) and cardiovascular disease (CVD). On the basis of predefined criteria (patient characteristics, genotype data format, allelic distribution, repeat length cutoff) 41 articles were selected. Patients were redistributed into 4 homogeneous subpopulations: patients with CVD (CVD group), patients without CVD (nonCVD), 'controls' with unknown cardiovascular status (unspecified) and children younger than 20 years of age (unselected). Genotype distributions (homozygous short [SS] or long [LL], and heterozygous) of the 4 patient categories were compared and odds ratios (ORs) for CVD were calculated using logistic regression analysis. Results: Overall, the proportion of the SS genotype was lower in CVD compared with nonCVD and unspecified. The ORs for CVD was highest in patients carrying the LL genotype (OR LL vs SS, 1.769 [95% confidence interval, 1.594-1.963]). Furthermore, genotype distribution differed between Caucasian and Asian individuals, the latter having a much higher proportion of the SS genotype (22% vs 11%). Conclusions: This review of the available literature on the epidemiological association between the HO-1 (GT) n repeat polymorphism and CVD supports the presumed protective effects of HO-1. The second but probably even more relevant finding of our review is that racial disparities in HO-1 (GT) n repeat length distribution exist and might influence the associations of the genotype with CVD status.
- 出版日期2016-2
