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内皮SRSF1通过ATF3-KLF2-S1PR1通路促进缺血诱导的血管生成
Wenting Zhu1,2,3, Ning Xie1, Zhenyan Li1
1Laboratory of Cardiovascular Science, Beijing Clinical Research Institute (W.Z., N.X., Z. Li, X.W., K.Z., R.D., L.G., Y.W., Y. Li, J.G., L.H., J.L., Y.J., W.A., Y. Liu, Z. Lin, C.-M.C.), Beijing Friendship Hospital, Capital Medical University, China.
Circulation research
|November 6, 2025
概括
氨酸/氨酸拼接因子1 (SRSF1) 通过调节ATF3-KLF2-S1PR1通路,促进外周动脉疾病中的血管生成. 调节SRSF1为缺血性血管疾病提供了潜在的治疗策略.
科学领域:
- 血管生物学 血管生物学
- 血管生成的分子机制
- 在RNA分离过程中.
背景情况:
- 周围动脉疾病 (PAD) 是一种严重的缺血性疾病,缺乏有效的药理疗法.
- 改善血管新生以恢复血液输液是PAD的关键治疗策略.
- 控制内皮细胞中缺血诱导血管生成的分子机制在很大程度上是未知的.
研究的目的:
- 为了确定缺血诱导血管生成的新型分子调节剂.
- 调查氨酸/氨酸拼接因子1 (SRSF1) 在内皮细胞功能和血管生成中的作用.
- 阐明SRSF1在对缺血反应中调节的下游信号通路.
主要方法:
- 发现驱动的蛋白质组分析,以确定内皮细胞中缺血反应蛋白.
- 在体内后肢缺血小鼠模型评估血管生成和血液流量恢复.
- 使用人类内皮细胞进行体外测试 (管道形成,迁移,发芽).
- 转录组测序,eCLIP-seq,RNA下拉和ChIP-qPCR来确定分子机制.
主要成果:
- 在缺血后,SRSF1表达在内皮细胞中升高,并对缺氧反应.
- 在小鼠模型中,内皮SRSF1缺乏会影响血管生成和血液流量恢复.
- 在体外和体内,SRSF1过度表达增强了内皮血管功能 (管道形成,迁移,发芽).
- SRSF1直接结合ATF3前mRNA,促进全长的ATF3和抑制KLF2-S1PR1信号,从而增强血管生成.
- 阿尔普拉斯塔迪尔激活了SRSF1信号,改善了内皮血管生成.
结论:
- SRSF1是缺血引起的血管新生的一个新型调节剂.
- 通过ATF3-KLF2-S1PR1通路,SRSF1可以增强内皮血管功能.
- 向内皮SRSF1为缺血性血管疾病提供了一个有前途的治疗途径.
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