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激活CXCR7可以限制动脉样硬化,并通过增加脂肪组织中的胆固醇吸收来改善高脂血症

Xiaofeng Li¹, Mengyu Zhu, Mark E Penfold

¹Institute for Molecular Cardiovascular Research (X.L., R.R.K., A.T., K.H., S.A., Z.W., M.v.Z., C.W., A.S.), Core Facility Two-Photon Imaging, Interdisciplinary Center for Clinical Research Aachen (S.K.), and Experimental Molecular Imaging (F.G., F.K.), RWTH Aachen University, Aachen, Germany; Institute for Cardiovascular Prevention, Ludwig Maximilians University Munich, Munich, Germany (M.Z., R.R.K., K.H., C.W., A.S.); ChemoCentryx Inc, Mountain View, CA (M.E.P., T.J.S.); Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands (M.v.Z., C.W.); and Munich Heart Alliance, Munich, Germany (C.W., A.S.).

|December 31, 2013

概括

化学因受体CXCR7 (C-X-C化学因受体7型) 在动脉样硬化中起着关键作用. 通过像CCX771这样的配体准CXCR7,可以降低胆固醇,并减少血管疾病的进展.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
代谢疾病代谢疾病

背景情况:

CXCR7 (C-X-C化学因子受体7型) 是CXCL12的替代受体.
CXCL12/CXCR7信号传导影响干细胞修复和动脉样硬化.
CXCR4是CXCL12的另一个受体,参与限制动脉样硬化.

研究的目的:

研究CXCR7在动脉样硬化和血管改造中的作用.
评估针对心血管疾病中CXCR7的治疗潜力.

主要方法:

在有条件CXCR7缺失的小鼠中,导线诱导的动脉损伤.
用合成CXCR7配体CCX771治疗高脂肪饮食中的阿波利波蛋白E缺陷 (Apoe(-/-)) 小鼠.
分析脂肪组织中新密度的形成,巨细胞的积累,脂蛋白水平和非常低密度脂蛋白 (VLDL) 的吸收.

主要成果:

对CXCR7的遗传删除加剧了neointima形成和受伤后的巨细胞积累.
在阿波小鼠中,CCX771治疗抑制了病变的发展,并改善了超脂血症.
CCX771减少了循环中的VLDL,增强了白色脂肪组织中的VLDL吸收,并降低了Angptl4表达.

结论:

CXCR7通过增强脂肪组织中VLDL吸收来调节血液中的胆固醇.
这种CXCR7的降胆固醇效应对动脉样硬化有好处,可能通过减少超脂血症诱导的单细胞化.
合成的CXCR7配体为动脉样硬化血管疾病提供治疗策略.

关键词:

动脉样硬化动脉样硬化冠状动脉静脉复缩症冠状动脉静脉复缩症超高胆固醇血症是一种高胆固醇血症.

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