■本研究旨在探讨循环炎症因子CRP水平,基于IL-6、IL-10和TNF-α的文献综述。这项研究还使用荟萃分析研究了单核苷酸多态性(SNP)位点对腹主动脉瘤(AAA)易感性的影响,并旨在提供有关AAA研究发病机理的其他信息。
■系统搜索了包括PubMed和WebofScience在内的电子数据库,以收集有关AAA的信息,炎症因子,如CRP,用于数据提取的IL-6、IL-10、TNF-α和SNP位点。总共评估了四个基因中的六个SNP(rs3091244,CRP;rs1800947,CRP;rs1205,CRP;rs1800795,IL-6;rs1800896,IL-10;和rs1800629,TNF)。
本研究共纳入41项相关调查,涉及9,007例AAA患者进行荟萃分析。根据汇总分析,循环CRP和IL-6水平显示与AAA相关,而血浆IL-10和TNF-α水平与AAA无关。循环CRP水平标准均差(SMD)为0.30(95%置信区间(CI):0.17-0.43),IL-6水平SMD为0.34(95%CI:0.20-0.49),IL-10水平SMD为-0.01(95%CI:-0.09-0.06),TNF-α水平SMD为0.09(95%CI:0.00-0.19)。同样,rs3091244(CRP)在隐性基因模型下的比值比(OR)为1.70(95%CI:1.13-2.57)。此外,在rs3091244位点具有A和T突变基因的个体可能比具有C等位基因的个体具有更高的AAA易感性趋势。连续,等位基因模型中rs1800795(IL-6)基因座的OR为0.91(95%CI:0.51-0.97),与具有C等位基因的个体相比,在rs1800795(IL-6)基因座具有G突变基因的个体对AAA的敏感性较低。同时,rs1800896(IL-10)位点在五个统计模型下呈正相关,并且在rs1800896位点具有A突变基因的个体对AAA的易感性可能高于具有G等位基因的个体。然而,rs1800947(CRP),rs1205(CRP),和rs1800629(TNF)位点在5个统计模型下不存在正相关,没有统计学意义。结果表明,rs1800629,rs1800947和rs1205位点的基因多态性与AAA易感性无关。
■某些已知的与AAA易感性相关的炎症介质中的基因多态性可能作为临床应用的潜在预测生物标志物。此外,与腹主动脉瘤形成和进展相关的炎症介质的SNP需要广泛的研究来证实这些结果。
UNASSIGNED: This study aimed to explore the levels of circulating inflammatory factors CRP, IL-6, IL-10 and TNF- α based on the literature review. This study also examined the influence of single nucleotide polymorphism (SNP) sites on the susceptibility of abdominal aortic aneurysm (AAA) using meta-analysis and intended to provide additional information on pathogenesis of AAA research.
UNASSIGNED: Electronic databases including PubMed and Web of Science were systemically searched to collect the information on AAA, inflammatory factors such as CRP, IL-6, IL-10, TNF- α and the SNP sites for data extraction. Altogether six SNPs in four genes (rs3091244, CRP; rs1800947, CRP; rs1205, CRP; rs1800795, IL-6; rs1800896, IL-10; and rs1800629, TNF) were assessed.
UNASSIGNED: This study enrolled altogether 41 relevant investigations involving 9,007 AAA patients to carry out meta-analysis. According to pooled analysis, circulating CRP and IL-6 levels were shown to be related to the AAA, while plasma IL-10 and TNF- α levels were not associated with AAA. The circulating CRP level standard mean difference (SMD) was 0.30 (95% confidence interval (CI): 0.17-0.43), the IL-6 level SMD was 0.34 (95% CI: 0.20-0.49), the IL-10 level SMD was -0.01 (95% CI: -0.09-0.06), and the TNF- α level SMD was 0.09 (95% CI: 0.00-0.19). Similarly, the odds ratio (OR) of rs3091244 (CRP) under the recessive gene model was 1.70 (95% CI: 1.13-2.57). In addition, individuals with A and T mutant genes at locus rs3091244 might have a higher tendency of AAA susceptibility than those with C allele. Consecutively, the OR was 0.91 (95% CI: 0.51-0.97) for rs1800795 (IL-6) locus in the allele model, and individuals with G mutant gene at locus rs1800795 (IL-6) might be less susceptible to AAA than those with C allele. Meanwhile, the rs1800896 (IL-10) locus had a positive association under the five statistical models, and individuals with A mutant gene at locus rs1800896 might have a higher susceptibility to AAA than those with G allele. Nevertheless, the rs1800947 (CRP), rs1205 (CRP), and rs1800629 (TNF) loci did not have positive correlation under the five statistical models, with no statistical significance. The results indicate that the gene polymorphisms at rs1800629, rs1800947, and rs1205 loci were not related to the AAA susceptibility.
UNASSIGNED: Gene polymorphisms in certain known inflammatory mediators related to AAA susceptibility might serve as potential predictive biomarkers for clinical applications. Moreover, SNP of inflammatory mediators relevant to abdominal aortic aneurysmal formation and progression need extensive investigations to confirm these results.