Proresolving receptor tames inflammation in atherosclerosis.
Proresolving receptor tames inflammation in atherosclerosis.
复制标题
促解受体可抑制动脉粥样硬化中的炎症。
DOI：
10.1172/jci155240
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Spite,Matthew
中科院分区：
文献类型：
--
作者：
Mena,HebeAgustina;Spite,Matthew
不解决的炎症有助于动脉粥样硬化的进展，动脉粥样硬化是一种慢性疾病，其特征是富含脂质的动脉斑块浸润免疫细胞的积累。在这一期的jci中，Arnardottir和Thul等人报道了GPR32（一种促进脂质介质包括resolvin D1的受体）在人类动脉粥样硬化病变中减少，并且该受体在小鼠中的过表达减少了动脉粥样硬化斑块的病变面积和坏死。在机制上，GPR32信号通路减弱了促炎细胞因子的产生，增强了巨噬细胞的吞噬作用，减少了白细胞的积累。这些结果表明，靶向治疗GPR32可能是解决动脉粥样硬化慢性炎症的一种方法。
Nonresolving inflammation contributes to the progression of atherosclerosis, a chronic disease characterized by the accumulation of lipid-rich arterial plaques infiltrated with immune cells. In this issue of theJCI, Arnardottir and Thul et al. report that GPR32, a receptor for proresolving lipid mediators including resolvin D1, was decreased in human atherosclerotic lesions and that overexpression of this human receptor in mice reduced lesion area and necrosis of atherosclerotic plaques. Mechanistically, GPR32 signaling blunted the production of proinflammatory cytokines, enhanced macrophage phagocytosis, and reduced leukocyte accumulation. These results suggest that therapeutic targeting of GPR32 could be an approach to resolving chronic inflammation in atherosclerosis.