...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell death & disease. >Egg antigen p40 of Schistosoma japonicum promotes senescence in activated hepatic stellate cells by activation of the STAT3/p53/p21 pathway
【24h】

Egg antigen p40 of Schistosoma japonicum promotes senescence in activated hepatic stellate cells by activation of the STAT3/p53/p21 pathway

机译：日本血吸虫的卵抗原p40通过激活STAT3 / p53 / p21途径促进活化的肝星状细胞的衰老

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Liver fibrosis is a serious disease that is characterized by the excess deposition of extracellular matrix (ECM) components. Activated hepatic stellate cells (HSCs) are a major source of ECM and serve as a key regulator in liver fibrogenesis. Inactivation of HSCs is essential for liver fibrotic regression. The present study explores the underlying mechanisms of Schistosoma japonicum egg antigen p40 (Sjp40) promoting senescence in HSCs and antifibrosis. For the first time we report that Sjp40 inhibits the activation and proliferation of an immortalized human HSC line (LX-2 cells) and promotes cellular senescence and cell cycle arrest. Sjp40 through action on the STAT3/p53/p21 pathway triggered cellular senescence, while knockdown of p53 or STAT3 partly restored cell senescence. In addition, Sjp40-induced cellular senescence caused LX-2 cells to be more sensitive to a human NK cell line (YT cells). Together these findings provide novel insights into the mechanism of antifibrosis and may have implications for the development of antifibrosis therapies.
机译：肝纤维化是一种严重的疾病，其特征是细胞外基质（ECM）成分过多沉积。活化的肝星状细胞（HSC）是ECM的主要来源，并且是肝纤维化的关键调节剂。 HSC的失活对于肝纤维化消退至关重要。本研究探讨了日本血吸虫卵抗原p40（Sjp40）促进HSCs衰老和抗纤维化的潜在机制。我们首次报道Sjp40抑制永生化人类HSC系（LX-2细胞）的活化和增殖，并促进细胞衰老和细胞周期停滞。 Sjp40通过作用于STAT3 / p53 / p21途径触发了细胞衰老，而敲除p53或STAT3则部分恢复了细胞衰老。此外，Sjp40诱导的细胞衰老导致LX-2细胞对人NK细胞系（YT细胞）更加敏感。这些发现共同为抗纤维化的机理提供了新颖的见解，并可能对抗纤维化疗法的发展产生影响。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
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