2013
DOI: 10.1016/j.atherosclerosis.2013.03.032
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Mediation analysis reveals a sex-dependent association between ABO gene variants and TG/HDL-C ratio that is suppressed by sE-selectin level

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Cited by 29 publications
(33 citation statements)
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“…In several clinical researches as well as studies investigating the effects of genetic variants [29][30][31], mediation analysis has been used to assess an intermediate variable as a mediator in the pathway between a risk factor and an outcome to estimate the extent to which the effect of the risk factor occurs through the mediator. In the current study, we performed this analysis and specifically found that both sdLDL-C and large HDL-C were partly mediated this relationship, however, only 8.7-10.5% effect size has been mediated, which may suggest that SUA probably plays an important role in the development of CAD by itself or through other pathways.…”
Section: Tablementioning
confidence: 99%
“…In several clinical researches as well as studies investigating the effects of genetic variants [29][30][31], mediation analysis has been used to assess an intermediate variable as a mediator in the pathway between a risk factor and an outcome to estimate the extent to which the effect of the risk factor occurs through the mediator. In the current study, we performed this analysis and specifically found that both sdLDL-C and large HDL-C were partly mediated this relationship, however, only 8.7-10.5% effect size has been mediated, which may suggest that SUA probably plays an important role in the development of CAD by itself or through other pathways.…”
Section: Tablementioning
confidence: 99%
“…For instance, variants of the ABO and CDH13 genes (which encode the ABO histo-blood group antigen and glycosylphosphatidylinositol-anchored cadherin 13, respectively) were reported to associate with sICAM1 levels [10, 17, 18]. Recently, a GWAS identified and localized the genetic determinants of sICAM1 levels to several loci in the genome, including two SNPs, rs3136642 and rs1049728, in the NFKBIK and RELA genes which function in the NF-κB pathway [11].…”
Section: Introductionmentioning
confidence: 99%
“…As possible links between ABO blood groups and CAD pathogenesis, previous studies have emphasized the increased prothrombotic state, higher prevalence of traditional cardiovascular risk factors, and higher level of systemic inflammatory response revealed in patients with different ABO blood groups [3][4][5]. Recently, genome-wide association studies (GWAS) have revealed significant associations of genetic variants in the ABO blood group region with levels of various inflammatory markers, including soluble levels of E-selectin (sE-selectin), intercellular adhesive molecule 1 (ICAM1), and P-selectin (sP-selectin) [6].…”
mentioning
confidence: 99%