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Vascular endothelial S1pr1 ameliorates adverse cardiac remodeling via stimulating reparative macrophage proliferation after myocardial infarction.
Cardiovascular Research ( IF 10.8 ) Pub Date : 2020-02-24 , DOI: 10.1093/cvr/cvaa046
Yashu Kuang 1 , Xiaolin Li 2 , Xiuxiang Liu 1 , Lu Wei 1 , Xiaoli Chen 1 , Jie Liu 1 , Tao Zhuang 1 , Jingjiang Pi 1 , Yanfang Wang 1 , Chenying Zhu 3 , Xin Gong 3 , Hao Hu 3 , Zuoren Yu 1 , Jiming Li 1 , Ping Yu 3 , Huimin Fan 3 , Yuzhen Zhang 1 , Zhongmin Liu 1 , Lin Zhang 1
Affiliation  

Endothelial cell (EC) homoeostasis plays an important role in normal physiological cardiac functions, and its dysfunction significantly influences pathological cardiac remodelling after myocardial infarction (MI). It has been shown that the sphingosine 1-phosphate receptor 1 (S1pr1) was highly expressed in ECs and played an important role in maintaining endothelial functions. We thus hypothesized that the endothelial S1pr1 might be involved in post-MI cardiac remodelling.

中文翻译:

血管内皮 S1pr1 通过刺激心肌梗死后修复性巨噬细胞增殖来改善不利的心脏重塑。

内皮细胞(EC)稳态在正常生理心脏功能中起重要作用,其功能障碍显着影响心肌梗死(MI)后的病理性心脏重构。已经表明,鞘氨醇 1-磷酸受体 1 (S1pr1) 在 ECs 中高表达,并在维持内皮功能方面发挥重要作用。因此,我们假设内皮 S1pr1 可能参与 MI 后心脏重塑。
更新日期:2020-02-24
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