...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of cellular physiology. >Nur77 deficiency exacerbates cardiac fibrosis after myocardial infarction by promoting endothelial-to-mesenchymal transition
【24h】

Nur77 deficiency exacerbates cardiac fibrosis after myocardial infarction by promoting endothelial-to-mesenchymal transition

机译：Nur77缺乏加剧心脏纤维化心肌梗死后推广endothelial-to-mesenchymal过渡

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Cardiac fibrosis is a reparative process after myocardial infarction (Ml), which leads to cardiac remodeling and finally heart failure. Endothelial-to-mesenchymal transition (EndMT) is induced after Ml and contributes to cardiac fibrosis after Ml. Orphan nuclear receptor Nur77 is a key regulator of inflammation, angiogenesis, proliferation, and apoptosis in vascular endothelial cells. Here, we investigated the role of orphan nuclear receptor Nur77 in EndMT and cardiac fibrosis after Ml. Cardiac fibrosis was induced through Ml by ligation of the left anterior descending coronary artery. We demonstrated that Nur77 knockout aggravated cardiac dysfunction and cardiac fibrosis 30 days after Ml. Moreover, Nur77 deficiency resulted in enhanced EndMT as shown by increased expression of FSP-1, SM22alpha, Snail, and decreased expression of PECAM-1 and eNOS compared with wild-type mice after MI. Then, we found overexpression Nur77 in human coronary artery endothelial cells significantly inhibited interleukin 1beta and transforming growth factor beta2-induced EndMT, as shown by a reduced transition to a fibroblast-like phenotype and preserved angiogenesis potential. Mechanistically, we demonstrated that Nur77 downregulated EndMT by inhibiting the nuclear factor-kappaB-dependent pathway. In conclusion, Nur77 is involved in cardiac fibrosis by inhibiting EndMT and may be a promising target for therapy of cardiac fibrosis after MI.
机译：心肌纤维化是一个修复的过程心肌梗死(Ml),导致心脏重构,最后心脏衰竭。Endothelial-to-mesenchymal过渡(EndMT)毫升后诱导,有助于心脏毫升。孤儿核受体Nur77后纤维化是一个关键调节器的炎症,血管生成,增殖和凋亡在血管内皮细胞。孤儿核受体Nur77 EndMT和心脏纤维化后毫升。心脏纤维化结扎诱导通过Ml的左边冠状动脉前降。证明Nur77淘汰赛加剧心脏功能障碍和心脏纤维化30天毫升。此外,Nur77不足导致增强EndMT如图所示的表达增加FSP-1, SM22alpha、蜗牛和减少表达PECAM-1和以挪士相比之下野生型老鼠MI后。然后,我们发现超表达Nur77人类冠状动脉内皮细胞显著抑制白介素- 1β和转化生长因子减少beta2-induced EndMT,如图所示过渡到一个呈表型保护血管生成潜力。从力学上看,我们证明了Nur77表达下调EndMT通过抑制核factor-kappaB-dependent途径。Nur77参与心脏纤维化抑制EndMT和可能是一个有前途的目标在心肌梗死后心脏纤维化的治疗。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号