Chemokines in cardiac fibrosis.

Chemokines in cardiac fibrosis.
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心脏纤维化中的趋化因子。

DOI:
10.1016/j.cophys.2020.10.004
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发表时间:
2021-03
影响因子:
2.5
通讯作者:
Frangogiannis NG
Frangogiannis NG
中科院分区:
其他
文献类型:
--
作者:
Li R;Frangogiannis NG

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趋化因子家族的几个成员参与纤维化的调节。这篇综述手稿讨论了趋化因子在心肌纤维化发病机制中的作用。 CC 趋化因子 CCL2 通过招募和激活表达其受体 CCR2 的单核细胞和巨噬细胞来发挥纤维化作用。其他 CC 趋化因子也可能通过招募纤维化巨噬细胞亚群来促进纤维化重塑。含有 ELR 基序的 CXC 趋化因子可能通过招募活化的中性粒细胞并随后形成中性粒细胞胞外陷阱 (NET) 或通过激活纤维化单核细胞来发挥促纤维化作用。 CXCL12 还被认为可以通过对成纤维细胞和免疫细胞的影响来发挥纤维形成作用。相反,CXCR3 配体 CXCL10 被发现可以减少心脏纤维化,抑制成纤维细胞迁移。趋化因子是心肌疾病中炎症和纤维化之间的关键联系,可能是伴有明显炎症和纤维化的心力衰竭患者的有希望的治疗靶点。
Several members of the chemokine family are involved in regulation of fibrosis. This review manuscript discusses the role of the chemokines in the pathogenesis of myocardial fibrosis. The CC chemokine CCL2 exerts fibrogenic actions through recruitment and activation of monocytes and macrophages expressing its receptor, CCR2. Other CC chemokines may also contribute to fibrotic remodeling by recruiting subsets of fibrogenic macrophages. CXC chemokines containing the ELR motif may exert pro-fibrotic actions, through recruitment of activated neutrophils and subsequent formation of neutrophil extracellular traps (NETs), or via activation of fibrogenic monocytes. CXCL12 has also been suggested to exert fibrogenic actions through effects on fibroblasts and immune cells. In contrast, the CXCR3 ligand CXCL10 was found to reduce cardiac fibrosis, inhibiting fibroblast migration. Chemokines are critical links between inflammation and fibrosis in myocardial disease and may be promising therapeutic targets for patients with heart failure accompanied by prominent inflammation and fibrosis.
DOI: 10.1080/25787489.2020.1719319
发表时间: 2019-09-03
影响因子: 1.6
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