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瑞索尔D2/GPR 18轴通过抑制促炎性巨细胞两极分化来改善压力过载引起的心力衰竭

Zihui Zheng¹, Mengmeng Zhao¹, Yao Xu¹

¹Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China.

Journal of lipid research

|November 4, 2024

概括

瑞索尔D2 (RvD2) 通过减少炎症和改善心脏功能来预防心力衰竭 (HF). 这种效应通过其受体G蛋白结合受体18 (GPR18) 介导,涉及调节巨细胞两极分化.

科学领域:

心血管生物学心血管生物学
炎症研究炎症研究
脂质介质信号传递信号传递

背景情况:

慢性炎症是心力衰竭 (HF) 发病的关键驱动因素.
像Resolvin D2 (RvD2) 这样的专门的亲溶解脂质调解剂 (SPM) 通过促进溶解,以其在疾病中的保护作用而闻名.
在HF的背景下RvD2的特定作用仍然在很大程度上未被探索.

研究的目的:

调查RvD2在压力过载引起的心力衰竭 (HF) 中的作用.
阐明底层机制,包括其受体G蛋白结合受体18 (GPR18) 的参与.
评估RvD2/GPR18轴作为HF治疗策略的潜力.

主要方法:

利用小鼠模型的压力过载诱导的HF.
接受了RvD2治疗,并评估了心脏重塑和功能.
在Gpr18缺乏的小鼠和骨髓移植实验中研究了GPR18的作用.
在体内和体外使用骨髓衍生巨细胞 (BMDMs) 分析了炎症反应,巨细胞极化 (高Ly6C) 和信号通路 (STAT1,NF-κB p65).

主要成果:

在HF小鼠中,RvD2治疗显著改善了心脏功能和减弱了心脏重塑.
RvD2的有益作用取决于GPR18的存在,因为Gpr18缺乏消除了这些效应.
RvD2抑制了炎症反应和Ly6C高巨分化,这是通过GPR18.
从机理上讲,RvD2抑制了巨细胞中的STAT1和NF-κB p65酸化,而这些效应由途径激动剂可逆.

结论:

RvD2/GPR18轴在缓解高频率心脏重塑和功能障碍方面发挥着至关重要的保护作用.
RvD2通过通过STAT1和NF-κB p65信号通路调节巨细胞表型来发挥其有益作用.
RvD2/GPR18轴通过利用其抗炎性质来管理心力衰竭,代表了一个有前途的治疗标.

关键词:

在 GPR18 中使用.心脏衰竭是因为心脏衰竭.巨细胞的两极分化压力过载的压力过载.解决了 D2 D2 的问题.

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