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基因多态性增加颅内动脉瘤风险:白细胞介素-1β-511C>T(第一部分)。

Gene Polymorphisms Increasing the Risk of Intracranial Aneurysms: Interleukin-1β -511C>T (Part I).

机构信息

Neurosurgery Unit, Department of Clinical-Surgical, Diagnostic and Pediatric Sciences, University of Pavia, Pavia, Italy.

Department of Neurological Surgery, Hospital San Fernando, Buenos Aires, Argentina.

出版信息

Acta Biomed. 2022 Mar 21;92(S4):e2021419. doi: 10.23750/abm.v92iS4.12668.

DOI:10.23750/abm.v92iS4.12668
PMID:35441612
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9179052/
Abstract

Introduction Intracranial aneurysms (IAs) are devastating cerebrovascular diseases with multifactorial etiology. The role of inflammation is indisputable, and interleukins are pivotal in supporting local inflammatory pathways and endothelial dysfunction at the aneurysm wall. In the light of insufficient evidence reported in the literature, this meta-analysis was aimed to investigate the genetic linkage between IL-1β (rs16944) -511C>T polymorphisms and IAs susceptibility. Methods A comprehensive online literature review was completed using the PubMed/Medline and Web of Science databases in accordance with the PRISMA guidelines. "Interleukin-1β," "IL-1β," "polymorphism," "intracranial aneurysm," and "subarachnoid hemorrhage" were the main keywords. Only human case-control studies, published from 2005 to 2021, written in English or translated, were screened. In the statistical analysis, we applied the fixed- and random-effect models, according to the level of heterogeneity, to assess the odds ratios (ORs) and 95% confidence intervals (CIs). RevMan 5.0 software was used for the statistics. Results Only 4 studies were eligible, with a total of 2070 patients, 1050 of which were assigned to the study group. Combined results showed a statistically significant association between the risk of IAs and -511CC (OR=0.79, 95% CI [0.65-0.95], p=0.01), and CT (OR=0.69, 95% CI [0.58-0.82], p<0.0001; OR=0.71, 95% CI [0.55-0.93], p=0.01) allele variations, both in the fixed- and random- models. No correlation was identified for the -511TT genotype (p=0.42; p=0.78). All the texts showed a low level of publication bias. Conclusion The present meta-analysis proved a potential role of IL-1β -511CC/CT genotypes in the pathogenesis of IAs. Additional studies are imperative to explain the underlying neuroimmune mechanisms, also allowing tailoring the potential inflammatory-target therapies for IAs.

摘要

介绍

颅内动脉瘤(IA)是一种具有多因素病因的毁灭性脑血管疾病。炎症的作用是不可否认的,白细胞介素在支持局部炎症途径和动脉瘤壁内皮功能障碍方面起着关键作用。鉴于文献报道的证据不足,本荟萃分析旨在研究白细胞介素 1β(rs16944)-511C>T 多态性与 IA 易感性的遗传关联。

方法

根据 PRISMA 指南,使用 PubMed/Medline 和 Web of Science 数据库进行全面的在线文献综述。“白细胞介素-1β”、“IL-1β”、“多态性”、“颅内动脉瘤”和“蛛网膜下腔出血”是主要关键词。仅筛选 2005 年至 2021 年发表的、以英文或翻译形式发表的人类病例对照研究。在统计分析中,我们根据异质性水平应用固定效应和随机效应模型来评估比值比(ORs)和 95%置信区间(CIs)。使用 RevMan 5.0 软件进行统计。

结果

只有 4 项研究符合条件,共 2070 例患者,其中 1050 例被分配到研究组。综合结果表明,-511CC(OR=0.79,95%CI[0.65-0.95],p=0.01)和 CT(OR=0.69,95%CI[0.58-0.82],p<0.0001;OR=0.71,95%CI[0.55-0.93],p=0.01)等位基因变异与 IA 风险之间存在统计学显著关联,两种模型均如此。-511TT 基因型无相关性(p=0.42;p=0.78)。所有文本均显示出低水平的发表偏倚。

结论

本荟萃分析证明了白细胞介素 1β-511CC/CT 基因型在 IA 发病机制中的潜在作用。需要进一步的研究来解释潜在的神经免疫机制,也可以为 IA 量身定制潜在的炎症靶向治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/f23a16eecd1e/ACTA-92-419-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/38492d5b76bb/ACTA-92-419-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/c12cd55dcf22/ACTA-92-419-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/da47abe85811/ACTA-92-419-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/5c8149d094c7/ACTA-92-419-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/f23a16eecd1e/ACTA-92-419-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/38492d5b76bb/ACTA-92-419-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/c12cd55dcf22/ACTA-92-419-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/da47abe85811/ACTA-92-419-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/5c8149d094c7/ACTA-92-419-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7402/9179052/f23a16eecd1e/ACTA-92-419-g005.jpg

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