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

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.

Evaluation of physiological risk factors, oxidant-antioxidant imbalance, proteolytic and genetic variations of matrix metalloproteinase-9 in patients with pressure ulcer.

Pressure ulcer (PU) remains a common worldwide problem in all health care settings, it is synonymous with suffering. PU is a complex disease that is dependent on a number of interrelated factors. It involves multiple mechanisms such as physiological risk factors, chronic inflammation, oxidant-antioxidant imbalance and proteolytic attack on extracellular matrix by matrix metalloproteinases (MMP). Therefore, we propose that these wounds lead to molecular variations that can be detected by assessing biomarkers. In this study, we aimed to evaluate the major clinical elements and biological scars in Tunisian patients suffering from PU. Consistently, non-healing wound remains a challenging clinical problem. The complex challenges of the wound environment, involving nutrient deficiencies, bacterial infection, as well as the critical role played by inflammatory cells, should be considered because of their negative impact on wound healing. In addition, an imbalance between pro-oxidants and antioxidant systems seems to be more aggravated in patients with PU compared to healthy subjects. Of interest, this study provides further evidence to support a core role of the biological activity of MMP-9 in the pathogenesis of PU and indicates that the MMP9-1562 C/T (rs 3918242) functional polymorphism is associated with protection against this disease.