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ADAMTS-7 基因多态性与冠心病易感性的关联:系统评价和荟萃分析。

Association of polymorphisms in ADAMTS-7 gene with the susceptibility to coronary artery disease - a systematic review and meta-analysis.

机构信息

Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.

Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.

出版信息

Aging (Albany NY). 2020 Oct 29;12(20):20915-20923. doi: 10.18632/aging.104118.

DOI:10.18632/aging.104118
PMID:33122452
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7655211/
Abstract

OBJECTIVE

To systematically review literature evidence to discover the association of ADAMTS7 (A Disintegrin And Metalloproteinase with Thrombospondin-like motifs 7) polymorphisms and the risk of developing CAD (coronary artery disease).

DATA SOURCES

A related literature search in online databases, including EMBASE, PubMed, and Web of Science was undertaken. The period covered was from 2007 to September 10, 2019.

RESULTS

Of 256 citations retrieved, nine relevant studies were selected for detailed evaluation. Five SNPs (rs3825807, rs1994016, rs4380028, rs79265682, and rs28455815) in ADAMTS7 gene were identified among included studies. There were 51,851 cases and 89,998 controls included in four studies for SNP rs3825807, 13,403 cases and 11,381 controls included in two studies for SNP rs1994016, 37,838 cases and 38,245 controls included in two studies for SNP rs4380028, 3,133 cases and 5,423 controls included in one study for SNP rs79265682, 103,494 cases and 198,684 controls included in one study for SNP rs28455815. We found most consistent evidence for an association with CAD on coronary angiogram with ADAMTS7 SNP rs3825807 risk allele A in contrast to control G allele, followed by rs4380028 (C vs. T allele), and rs1994016 (C vs. T allele).

CONCLUSIONS

ADAMTS7 polymorphism is likely an important risk factor for development of CAD. Our data also suggest that the ADAMTS7 polymorphism may be a risk factor for CAD progression in patients who already have pathology in their coronary arteries.

REVIEW METHODS

We included all studies in English language that reported correlation between the ADAMTS7 polymorphism and CAD in human cases.

摘要

目的

系统回顾文献证据,发现 ADAMTS7(解整合素和金属蛋白酶与血小板反应蛋白样结构域 7)多态性与 CAD(冠状动脉疾病)发病风险的关联。

资料来源

在 EMBASE、PubMed 和 Web of Science 等在线数据库中进行了相关文献检索。检索时间截至 2019 年 9 月 10 日。

结果

在 256 条引文检索中,选择了 9 项相关研究进行详细评估。在纳入的研究中确定了 ADAMTS7 基因中的 5 个 SNP(rs3825807、rs1994016、rs4380028、rs79265682 和 rs28455815)。四项研究纳入了 51851 例病例和 89998 例对照用于 SNP rs3825807,两项研究纳入了 13403 例病例和 11381 例对照用于 SNP rs1994016,两项研究纳入了 37838 例病例和 38245 例对照用于 SNP rs4380028,一项研究纳入了 3133 例病例和 5423 例对照用于 SNP rs79265682,一项研究纳入了 103494 例病例和 198684 例对照用于 SNP rs28455815。我们发现 ADAMTS7 SNP rs3825807 的风险等位基因 A 与对照 G 等位基因相比,与 CAD 冠状动脉造影最一致,其次是 rs4380028(C 与 T 等位基因)和 rs1994016(C 与 T 等位基因)。

结论

ADAMTS7 多态性可能是 CAD 发病的重要危险因素。我们的数据还表明,ADAMTS7 多态性可能是冠状动脉已有病变的患者 CAD 进展的危险因素。

综述方法

我们纳入了所有以人类病例为对象,报告 ADAMTS7 多态性与 CAD 相关性的英文研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/47158631758d/aging-12-104118-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/9685a4a045d2/aging-12-104118-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/1b9c800a3885/aging-12-104118-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/5345356cf170/aging-12-104118-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/47158631758d/aging-12-104118-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/9685a4a045d2/aging-12-104118-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/1b9c800a3885/aging-12-104118-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/5345356cf170/aging-12-104118-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c89e/7655211/47158631758d/aging-12-104118-g004.jpg

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Circ Genom Precis Med. 2020 Jun;13(3):e002670. doi: 10.1161/CIRCGEN.119.002670. Epub 2020 May 29.
2
Genetic variants of confer risk for ischaemic stroke in the Chinese population.基因变异在中国人群中会增加缺血性中风的风险。 (原英文句子表述不太完整,推测完整句子可能是“Genetic variants of some genes confer risk for ischaemic stroke in the Chinese population.”,翻译仅供参考,需结合完整准确的原文进行理解。)
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3
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Genes (Basel). 2023 Feb 16;14(2):508. doi: 10.3390/genes14020508.
4
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Biomolecules. 2022 Jul 8;12(7):959. doi: 10.3390/biom12070959.
5
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Medicine (Baltimore). 2020 Dec 11;99(50):e23652. doi: 10.1097/MD.0000000000023652.
Mechanisms and Consequences of Defective Efferocytosis in Atherosclerosis.
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Front Cardiovasc Med. 2018 Jan 8;4:86. doi: 10.3389/fcvm.2017.00086. eCollection 2017.
4
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5
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