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STrengthening the REporting of Genetic Association Studies (STREGA)--an extension of the STROBE statement.加强遗传关联研究报告规范（STREGA）--STROBE 声明的扩展。
Genet Epidemiol. 2009 Nov;33(7):581-98. doi: 10.1002/gepi.20410.
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Chemokines in atherosclerosis: an update.动脉粥样硬化中的趋化因子：最新进展
Arterioscler Thromb Vasc Biol. 2008 Nov;28(11):1897-908. doi: 10.1161/ATVBAHA.107.161174. Epub 2008 Jun 19.
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Estimating haplotype effects on dichotomous outcome for unphased genotype data using a weighted penalized log-likelihood approach.使用加权惩罚对数似然法估计未分型基因型数据对二分结果的单倍型效应。
Hum Hered. 2006;61(2):104-10. doi: 10.1159/000093476. Epub 2006 May 24.
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The many roles of chemokines and chemokine receptors in inflammation.趋化因子和趋化因子受体在炎症中的多种作用。
N Engl J Med. 2006 Feb 9;354(6):610-21. doi: 10.1056/NEJMra052723.
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Circulating levels of MCP-1 and eotaxin are not associated with presence of atherosclerosis or previous myocardial infarction.
Atherosclerosis. 2005 Dec;183(2):268-74. doi: 10.1016/j.atherosclerosis.2004.11.028.
7
Association among plasma levels of monocyte chemoattractant protein-1, traditional cardiovascular risk factors, and subclinical atherosclerosis.血浆单核细胞趋化蛋白-1水平、传统心血管危险因素与亚临床动脉粥样硬化之间的关联。
J Am Coll Cardiol. 2004 Nov 2;44(9):1812-8. doi: 10.1016/j.jacc.2004.07.047.
8
Atherosclerosis in patients infected with HIV is influenced by a mutant monocyte chemoattractant protein-1 allele.感染HIV的患者的动脉粥样硬化受一种突变的单核细胞趋化蛋白-1等位基因影响。
Circulation. 2004 Oct 12;110(15):2204-9. doi: 10.1161/01.CIR.0000143835.95029.7D. Epub 2004 Oct 4.
9
Macrophage migration inhibitory factor and the risk of myocardial infarction or death due to coronary artery disease in adults without prior myocardial infarction or stroke: the EPIC-Norfolk Prospective Population study.巨噬细胞移动抑制因子与无既往心肌梗死或中风的成年人发生冠状动脉疾病所致心肌梗死或死亡风险：EPIC-诺福克前瞻性人群研究
Am J Med. 2004 Sep 15;117(6):390-7. doi: 10.1016/j.amjmed.2004.04.010.
10
Association of RANTES G-403A gene polymorphism with increased risk of coronary arteriosclerosis.RANTES基因G-403A多态性与冠状动脉粥样硬化风险增加的关联。
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趋化因子配体 2 基因变异、血清单核细胞趋化蛋白-1 水平与冠心病风险。

Chemokine ligand 2 genetic variants, serum monocyte chemoattractant protein-1 levels, and the risk of coronary artery disease.

机构信息

Department of Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands.

出版信息

Arterioscler Thromb Vasc Biol. 2010 Jul;30(7):1460-6. doi: 10.1161/ATVBAHA.110.205526. Epub 2010 Apr 29.

DOI:10.1161/ATVBAHA.110.205526
PMID:20431065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4210837/
Abstract

OBJECTIVE

In humans, evidence about the association between levels of monocyte chemoattractant protein-1 (MCP-1), its coding gene chemokine (C-C motif) ligand 2 (CCL2), and risk of coronary artery disease (CAD) is contradictory.

METHODS AND RESULTS

We performed a nested case-control study in the prospective EPIC-Norfolk cohort investigating the relationship between CCL2 single-nucleotide polymorphisms (SNPs), MCP-1 concentrations, and the risk of future CAD. Cases (n=1138) were apparently healthy men and women aged 45 to 79 years who developed fatal or nonfatal CAD during a mean follow-up of 6 years. Controls (n=2237) were matched by age, sex, and enrollment time. Using linear regression analysis no association between CCL2 SNPs and MCP-1 serum concentrations became apparent, nor did we find a significant association between MCP-1 serum levels and risk of future CAD. Finally, Cox regression analysis showed no significant association between CCL2 SNPs and the future CAD risk. In addition, we did not find any robust associations between the CCL2 haplotypes and MCP-1 serum concentration or future CAD risk.

CONCLUSIONS

Our data do not support previous publications indicating that MCP-1 is involved in the pathogenesis of CAD.

摘要

目的

在人类中，关于单核细胞趋化蛋白-1（MCP-1）水平与其编码基因趋化因子（C-C 基序）配体 2（CCL2）与冠心病（CAD）风险之间的关联的证据存在矛盾。

方法和结果

我们在前瞻性 EPIC-Norfolk 队列中进行了一项巢式病例对照研究，调查了 CCL2 单核苷酸多态性（SNP）、MCP-1 浓度与未来 CAD 风险之间的关系。病例（n=1138）为年龄在 45 至 79 岁之间、在平均 6 年的随访期间发生致命或非致命 CAD 的健康男性和女性。对照组（n=2237）按年龄、性别和入组时间匹配。使用线性回归分析，我们没有发现 CCL2 SNP 与 MCP-1 血清浓度之间存在关联，也没有发现 MCP-1 血清水平与未来 CAD 风险之间存在显著关联。最后，Cox 回归分析显示 CCL2 SNP 与未来 CAD 风险之间没有显著关联。此外，我们没有发现 CCL2 单倍型与 MCP-1 血清浓度或未来 CAD 风险之间存在任何可靠的关联。

结论

我们的数据不支持先前的出版物，即 MCP-1 参与 CAD 的发病机制。