In conclusion, the 301T>C polymorphism of the ASP gene that influences the serum triglycerides level in the Uygur population, is associated with the development of CHD, and the CC genotype might be a risk factor of CHD.
We studied the association of four polymorphisms in the ABCA1 gene (G1051A, G2706A, G2868A and -565C/T) with lipid profile and coronary artery disease.
In conclusion, common genetic variations of ABCA1 had a moderate influence on HDL-C levels and/or coronary heart disease in patients with T2D.These 2 effects were independent.
CONCLUSIONS This meta-analysis provides convincing evidence that polymorphism of ABCA1R219K is associated with susceptibility to CHD while the CRP +1059G/C polymorphism appears to have no correlation with susceptibility to CHD.
After adjustment for risk factors and clinical features, ABCA1 (p = 0.005) and SREBF2 (p = 0.010) gene expression were identified as independent predictors of CHD and severity.
This study suggests that three SNPs rs2230806, rs4149313, and rs9282541 in ABCA1 gene are significantly associated with susceptibility to CHD; further mechanism should be performed to be applied to drug research and development.
In conclusion, this meta-analysis suggests that K allele of ABCA1R219K polymorphism is a protective factor associated with decreased CHD susceptibility, but these associations vary in different ethnic populations.
Moreover, of the 8 sex-biased genes at these loci, 4 have been directly linked to monogenic disorders of lipid metabolism and show an expression profile in females (elevated expression of ABCA1, APOA5 and LDLR; reduced expression of LIPC) that is consistent with the lower female risk of coronary artery disease.
The ATP-binding cassette transporter A1 (ABCA1) mediates reverse cholesterol transport, polymorphisms have been shown to influence the levels of cholesterol and of HDL and the risk of coronary artery disease.
However, the expression of the low-density lipoprotein receptor and ATP-binding cassette transporter A1 was markedly increased, indicating that the beneficial effect of statins in allergic asthma and coronary artery disease was mediated, at least in part, by decreasing cholesterol biosynthesis and foam cell formation.
The K allele of the R219K variant was significantly more frequent in FH subjects without premature CHD (0.32, 95% CI 0.27 to 0.37) than in FH subjects with premature CHD (0.25, 95% CI 0.21 to 0.29) (p<0.05), suggesting that the genetic variant R219K in ABCA1 could influence the development and progression of atherosclerosis in FH subjects.
These results suggest that defective ABCA1 function in cholesterol-loaded macrophages is one potential contributor to the impaired RCT process and the increased coronary heart disease risk in subjects with familial low HDL.
In conclusion, the R219K polymorphism of ABCA1 was associated with altered lipoprotein levels and the R219K variant significantly modulated the HDL-C response to pravastatin in Chinese patients with CHD.
Our data confirm earlier observations that ABCA1R219K and V771M polymorphisms may be associated with a protective role against CHD and extend those to another important pathologic condition, namely stroke.