2014
DOI: 10.1016/j.ajhg.2014.01.013
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The IL-33-ST2L Pathway Is Associated with Coronary Artery Disease in a Chinese Han Population

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Cited by 7 publications
(15 citation statements)
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“…Together, this suggests these variants may influence EH susceptibility by controlling their own expression. Previous studies have confirmed this, and shown that rs11685424 and rs6543116 are associated with elevated EH risk and increased sST2 expression [19,22]. As noted, rs3821204 disrupts a putative miRNA binding site; therefore we predicted that this variant controls ST2 expression via a mechanism that is distinct compared with the three other SNPs.…”
Section: Association Between St2 Variants and Eh Risksupporting
confidence: 70%
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“…Together, this suggests these variants may influence EH susceptibility by controlling their own expression. Previous studies have confirmed this, and shown that rs11685424 and rs6543116 are associated with elevated EH risk and increased sST2 expression [19,22]. As noted, rs3821204 disrupts a putative miRNA binding site; therefore we predicted that this variant controls ST2 expression via a mechanism that is distinct compared with the three other SNPs.…”
Section: Association Between St2 Variants and Eh Risksupporting
confidence: 70%
“…In this case–control study, we found that the rs11685424 and rs6543116 genetic variations within the ST2 promoter region are associated with EH risk. These two variants modify transcriptional activity of the ST2 promoter . Thus, it is likely that the biological consequence of these genetic variants may influence EH susceptibility.…”
Section: Discussionmentioning
confidence: 99%
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“…Previous data have demonstrated the association between the distal promoter variants in ST2 and angiographic severity of CAD, and suggest that the IL-33/ST2L pathway might be genetically associated with CAD [22] . Moreover, IL33/ST2 pathway was significantly associated not only with patients with severe coronary stenosis, but with the subgroup of MI or revascularization, and affected the level of circulating IL-33 genetically [23] . Our study found no associations between the three kinds of SNPs and MI after adjustment for hypertension and DM.…”
Section: Discussionmentioning
confidence: 98%
“…Most of them, however, are located in the intron of IL‐33 and have no function. In this study, we focused on a functional polymorphism rs7025417 that are located in the promoter of IL‐33 (−1611 bp from the transcription start site), with the different genotypes affecting the levels of circulating IL‐33 . Because IL‐33 exerts functions via ST2, another SNP rs3821204 was selected, which was located within the 3′ untranslated region (UTR) of ST2 mRNA.…”
Section: Introductionmentioning
confidence: 99%