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白细胞介素-8及其受体CXCR2在动脉粥样硬化中的作用

Interleukin-8 and its receptor CXCR2 in atherosclerosis.

作者信息

Boisvert W A, Curtiss L K, Terkeltaub R A

机构信息

Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.

出版信息

Immunol Res. 2000;21(2-3):129-37. doi: 10.1385/ir:21:2-3:129.

Abstract

The participation of inflammatory cells in atherosclerosis is a well-known process that involves numerous molecules including chemotactic cytokines (chemokines) for their entry into the vessel wall. Although the C-C chemokine monocyte chemoattractant protein-1 and its receptor, CCR2, have been implicated in atherosclerosis, the role of the classic C-X-C chemokine, interleukin-8 (KC/growth-related oncogene alpha in mice) and its receptor CXCR2 has not been studied in the pathogenesis of atherosclerosis. Our research has shown that CXCR2 is strongly expressed on macrophages (Mphi) in atherosclerotic lesion. This CXCR2 expression is proatherogenic in that CXCR2 deficiency significantly reduces the progression of advanced atherosclerosis in mice. Although the mechanism still needs to be worked out, it appears that CXCR2 expression on lesion Mphi is essential for these cells to be retained in the lesion.

摘要

炎症细胞参与动脉粥样硬化是一个众所周知的过程,该过程涉及众多分子,包括趋化细胞因子(趋化因子),它们促使炎症细胞进入血管壁。虽然C-C趋化因子单核细胞趋化蛋白-1及其受体CCR2与动脉粥样硬化有关,但经典的C-X-C趋化因子白细胞介素-8(小鼠中的KC/生长相关癌基因α)及其受体CXCR2在动脉粥样硬化发病机制中的作用尚未得到研究。我们的研究表明,CXCR2在动脉粥样硬化病变中的巨噬细胞上强烈表达。这种CXCR2表达具有促动脉粥样硬化作用,因为CXCR2缺陷显著降低了小鼠晚期动脉粥样硬化的进展。虽然其机制仍有待阐明,但病变巨噬细胞上的CXCR2表达似乎对于这些细胞滞留在病变中至关重要。

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