Han Xia, Liang Xiaotang, Wu Menghai, Zhang Lijun, Jiang Honglei
Department of Cardiology, Jinan People's Hospital Affiliated to Shandong First Medical University, Laiwu, 271199, People's Republic of China.
Shandong Second Provincial General Hospital, Jinan, Shandong Province, 250000, People's Republic of China.
Pharmgenomics Pers Med. 2021 Aug 28;14:1081-1086. doi: 10.2147/PGPM.S324767. eCollection 2021.
To evaluate the associations of genetic variants of the miR-217 gene with coronary artery disease (CAD) risk, as well as plasma level of vascular endothelial growth factor (VEGF).
A case-control study with 498 CAD patients and 499 frequency-matched healthy controls was conducted to evaluate the associations of four tagSNPs of the miR-217 gene, including rs6724872, rs4999828, rs10206823, and rs41291177, with CAD risk and plasma level of VEGF.
SNP rs6724872 and rs4999828 were significantly associated with increased risk of CAD (P value was smaller than 0.05 even after Bonferroni multiple adjustment). Compared with the G allele, C allele of rs6724872 was significantly associated with 1.73-fold increased risk of CAD (95% CI: 1.25-2.39; P = 0.001). While C allele of rs4999828 was significantly associated with 1.75-fold increased risk of CAD, compared with T allele (95% CI: 1.34-2.29; P = 4 × 10). Meanwhile, rs6724872 and rs4999828 were also significantly associated with higher level of VEGF (P < 0.001).
These findings highlighted the important role of genetic variants of the miR-217 gene in the pathogenesis of CAD and potential targets for intervention.
评估miR - 217基因的遗传变异与冠状动脉疾病（CAD）风险以及血管内皮生长因子（VEGF）血浆水平之间的关联。
进行了一项病例对照研究，纳入498例CAD患者和499例频率匹配的健康对照，以评估miR - 217基因的四个标签单核苷酸多态性（tagSNP），即rs6724872、rs4999828、rs10206823和rs41291177，与CAD风险和VEGF血浆水平的关联。
SNP rs6724872和rs4999828与CAD风险增加显著相关（即使经过Bonferroni多重校正，P值仍小于0.05）。与G等位基因相比，rs6724872的C等位基因与CAD风险增加1.73倍显著相关（95%可信区间：1.25 - 2.39；P = 0.001）。而与T等位基因相比，rs4999828的C等位基因与CAD风险增加1.75倍显著相关（95%可信区间：1.34 - 2.29；P = 4×10）。同时，rs6724872和rs4999828也与较高水平的VEGF显著相关（P < 0.001）。
这些发现突出了miR - 217基因的遗传变异在CAD发病机制中的重要作用以及潜在的干预靶点。
