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单核细胞趋化蛋白-1/趋化因子(C-C 基序)配体 2 与冠状动脉斑块特征的相关性。

Correlation between monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2 and coronary plaque characteristics.

机构信息

Department of Cardiology, Heart Center of Henan Provincial People's Hospital, Central China Fuwai Hospital, Zhengzhou University, Zhengzhou 450003, China.

Department of Ultrasound, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

出版信息

Exp Biol Med (Maywood). 2020 Sep;245(15):1335-1343. doi: 10.1177/1535370220941424. Epub 2020 Jul 8.

DOI:10.1177/1535370220941424
PMID:32640896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7441351/
Abstract

Vulnerable plaques are plaques which are susceptible to rupture or thrombosis and trigger a series of adverse events such as coronary disorders. CCL2 is a soluble basic protein belonging to the CC subfamily. Previous studies have been investigated on the correlation between inflammatory factors and clinical events, but there are few studies on the correlation between CCL2 and plaque characteristics. Our study found that the high expression of CCL2 is involved in multiple processes in the genesis and progression of coronary artery disease, and would be a potential clinical prognostic indicator. In addition, high expression of CCL2 may be related to gene pathways such as Nod-like receptor signaling pathway, suggesting that CCL2 is involved in the inflammatory response and immune process of coronary artery disease.

摘要

易损斑块是指易于破裂或形成血栓并引发一系列不良事件(如冠状动脉疾病)的斑块。CCL2 是一种可溶性碱性蛋白,属于 CC 亚家族。先前的研究已经探讨了炎症因子与临床事件之间的相关性,但关于 CCL2 与斑块特征之间的相关性研究较少。我们的研究发现,CCL2 的高表达参与了冠状动脉疾病发生和进展的多个过程,可能成为一个有潜在临床预后价值的指标。此外,CCL2 的高表达可能与 Nod-like receptor 信号通路等基因通路有关,提示 CCL2 参与了冠状动脉疾病的炎症反应和免疫过程。

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本文引用的文献

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Circ J. 2017 Sep 25;81(10):1439-1446. doi: 10.1253/circj.CJ-16-1209. Epub 2017 Apr 29.
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The CCL2/CCR2 Axis Affects Transmigration and Proliferation but Not Resistance to Chemotherapy of Acute Myeloid Leukemia Cells.CCL2/CCR2轴影响急性髓系白血病细胞的迁移和增殖,但不影响其对化疗的耐药性。
PLoS One. 2017 Jan 3;12(1):e0168888. doi: 10.1371/journal.pone.0168888. eCollection 2017.
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