Genetic polymorphisms in VEGFA and VEGFR2 genes associated with coronary heart disease susceptibility and severity

Foddha Hajer,Saoud Hana, Chouchene Saoussen, Foddha Abdelhak,Bouzidi Nadia, Dhiflaoui Ameni,Gamra Habib, Ben abdennebi Hassen,Haj Khelil Amel

Molecular Biology Reports(2023)

引用 0|浏览2
暂无评分
摘要
Background ​Vascular endothelial growth factor A ( VEGFA ) is well acknowledged as a powerful angiogenesis-promoting agent mainly through its receptor VEGFR2 . Ischemia stimulates VEGFA / VEGFR2 signaling pathway and elevated serum levels of VEGFA were detected in coronary heart disease (CHD) patients. The goal of the current study is to determine how four SNPs in the genes for VEGFA (rs3025039 and rs699947) and VEGFR2 (rs2305948 and rs1870377) contribute to the development of CHD. We also wanted to use the Gensini score to confirm if these four SNPs have an effect on the severity of coronary lesions. Methods In this case-control research, we used the restriction fragment length polymorphism of the polymerase chain reaction to genotype 239 CHD patients and 200 controls. Age, sex, smoking behavior, and obesity were taken into account in the statistical analysis. Results Two VEGFA /VEFGR2 signaling pathway SNPs (rs699947 and rs1870377) were found to be associated with CHD (C vs. A, P = 0.002; OR = 1.47 (1.12–1.93); A vs. T, P = 0.001; OR = 1.58 (1.17–2.13) respectively). The rs2305948 showed no allelic associations with CHD susceptibility, although we noticed a slight association under the recessive model of rs3025039 TT genotype (p = 0.023; OR = 6.41 (1.14–36.12)) only under adjusted analyses. In addition, both VEGFA SNPs (rs699947and rs3025039) were found to be associated with high Gensini score (p < 0.001). Conclusions Our research helps to shed further light on the pathophysiology of CHD. The VEGFA / VEGFR2 signaling pathway may have been downregulated, increasing CHD susceptibility and risk.
更多
查看译文
关键词
VEGFA,VEGFR2,Coronary heart disease,Gensini score,Polymorphisms
AI 理解论文
溯源树
样例
生成溯源树,研究论文发展脉络
Chat Paper
正在生成论文摘要