The Association of Angiotensin Converting Enzyme and Angiotensinogen Gene Polymorphism With Dilated Cardiomyopathy: A Systematic Review and Meta-Analysis

血管紧张素转换酶和血管紧张素原基因多态性与扩张型心肌病的相关性:系统评价和荟萃分析

阅读:1

Abstract

BACKGROUND: Limited evidence exists for an association between dilated cardiomyopathy (DCM) and the angiotensin-converting enzyme (ACE) gene with an insertion/deletion (I/D) angiotensinogen (AGT) M235T gene polymorphism. A systematic review and meta-analysis were conducted to elucidate the role of ACE I/D and AGT M235T in the morbidity of DCM. This meta-analysis was performed following the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) 2020 guidelines for Abstracts. METHODS: The PubMed, Embase, and Cochrane Library databases, as well as the Chinese Biomedical Literature Database, were reviewed to identify and collect all relevant studies. The association between ACE I/D, AGT M235T gene polymorphism, and DCM was estimated by pooling the odds ratio (OR) using the RevMan5.4.1 and Stata12.0 software. RESULTS: A total of 27 eligible studies that explored the ACE I/D gene polymorphism in a healthy control group and the DCM patients were included in the present meta-analysis. A recessive genetic model was presented in the ACE I/D genotype. The pooled OR (DD vs. DI + II) following recessive genetic modelling was 1.37 (95% confidence interval (CI): 1.13, 1.66; p < 0.01). DCM patients tend to carry the DD genotype, indicating that the ACE I/D gene polymorphism might be associated with DCM. Similarly, seven studies were analyzed that presented a correlation between AGT M235T polymorphism and DCM morbidity. The OR (MT + TT vs. MM) value, according to a dominant genetic model, was 1.83 (95% CI: 0.90, 3.73; p > 0.05). CONCLUSION: The AGT M235T polymorphism was not significantly associated with DCM; however, the ACE I/D polymorphism was related to a risk of DCM.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。