Zhang Zhongwen, Wang Qiannan, Yao Jinming, Zhou Xiaojun, Zhao Junyu, Zhang Xiaoqian, Dong Jianjun, Liao Lin
Department of Endocrinology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, China.
Division of Endocrinology, Department of Internal Medicine, Shandong Provincial QianFoShan Hospital, Shandong University, Jinan, China.
Front Pharmacol. 2020 Mar 3;11:146. doi: 10.3389/fphar.2020.00146. eCollection 2020.
The key characteristic of cardiovascular disease (CVD) is endothelial dysfunction, which is likely the consequence of inflammation. It is well demonstrated that chemokines and their receptors play a crucial role in regulating inflammatory responses, and recently, much attention has been paid to chemokine receptor 5 (CCR5) and its ligands. For example, CCR5 aggravates the inflammatory response in adipose tissue by regulating macrophage recruitment and M1/M2 phenotype switch, thus causing insulin resistance and obesity. Inhibition of CCR5 expression reduces the aggregation of pro-atherogenic cytokines to the site of arterial injury. However, targeting CCR5 is not always effective, and emerging evidence has shown that CCR5 facilitates progenitor cell recruitment and promotes vascular endothelial cell repair. In this paper, we provide recent insights into the role of CCR5 and its ligands in metabolic syndrome as related to cardiovascular disease and the opportunities and roadblocks in targeting CCR5 and its ligands.
心血管疾病（CVD）的关键特征是内皮功能障碍，这很可能是炎症的结果。有充分证据表明，趋化因子及其受体在调节炎症反应中起关键作用，最近，趋化因子受体5（CCR5）及其配体受到了广泛关注。例如，CCR5通过调节巨噬细胞募集和M1/M2表型转换加剧脂肪组织中的炎症反应，从而导致胰岛素抵抗和肥胖。抑制CCR5表达可减少促动脉粥样硬化细胞因子在动脉损伤部位的聚集。然而，靶向CCR5并不总是有效，新出现的证据表明，CCR5促进祖细胞募集并促进血管内皮细胞修复。在本文中，我们提供了关于CCR5及其配体在与心血管疾病相关的代谢综合征中的作用以及靶向CCR5及其配体的机会和障碍的最新见解。
