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非典型趋化因子受体在心血管疾病中的作用

Atypical Chemokine Receptors in Cardiovascular Disease.

机构信息

Institute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.

German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.

出版信息

Thromb Haemost. 2019 Apr;119(4):534-541. doi: 10.1055/s-0038-1676988. Epub 2019 Feb 4.

DOI:10.1055/s-0038-1676988
PMID:30716778
Abstract

Inflammation has been well recognized as one of the main drivers of atherosclerosis development and therefore cardiovascular diseases (CVDs). It has been shown that several chemokines, small 8 to 12 kDa cytokines with chemotactic properties, play a crucial role in the pathophysiology of atherosclerosis. Chemokines classically mediate their effects by binding to G-protein-coupled receptors called chemokine receptors. In addition, chemokines can also bind to atypical chemokine receptors (ACKRs). ACKRs fail to induce G-protein-dependent signalling pathways and thus subsequent cellular response, but instead are able to internalize, scavenge or transport chemokines. In this review, we will give an overview of the current knowledge about the involvement of ACKR1-4 in CVDs and especially in atherosclerosis development. In the recent years, several studies have highlighted the importance of ACKRs in CVDs, although there are still several controversies and unexplored aspects that have to be further elucidated. A better understanding of the precise role of these atypical receptors may pave the way towards novel and improved therapeutic strategies.

摘要

炎症已被公认为动脉粥样硬化发展和心血管疾病(CVD)的主要驱动因素之一。研究表明,几种趋化因子,即具有趋化作用的 8 到 12 kDa 的小细胞因子,在动脉粥样硬化的病理生理学中起着至关重要的作用。趋化因子通过与称为趋化因子受体的 G 蛋白偶联受体结合来发挥其作用。此外,趋化因子还可以与非典型趋化因子受体(ACKR)结合。ACKR 不能诱导 G 蛋白依赖性信号通路和随后的细胞反应,而是能够内化、清除或转运趋化因子。在这篇综述中,我们将概述 ACKR1-4 参与 CVD 特别是动脉粥样硬化发展的最新知识。近年来,多项研究强调了 ACKR 在 CVD 中的重要性,尽管仍存在一些争议和未被探索的方面,需要进一步阐明。更好地了解这些非典型受体的确切作用可能为新的和改进的治疗策略铺平道路。

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