首页> 外文期刊>Gut: Journal of the British Society of Gastroenterology >NKT cells and the hedgehog pathway: An unhealthy marriage in non-alcoholic fatty liver disease?
【24h】

NKT cells and the hedgehog pathway: An unhealthy marriage in non-alcoholic fatty liver disease?

机译:NKT细胞和刺猬通路:非酒精性脂肪肝疾病中的不健康婚姻?

获取原文
获取原文并翻译 | 示例
           

摘要

In the progression of non-alcoholic fatty liver disease (NAFLD) to steatohepatitis (NASH), the hedgehog (Hh) pathway has recently been implicated, with a new target gene, osteopontin (OPN), being a candidate in the coordination of inflammation and fibrosis development. This pathway, which is critical in embryogenesis, can be activated in adult life in the context of tissue regeneration. It has been suggested that dying and injured hepatocytes, such as ballooned hepato-cytes,2 against a background of lipotox-icity, can produce Hh that will then act on inflammatory cells such as natural killer T (NKT) cells and on progenitor cells in such a way as to promote growth and hepatocyte differentiation, maintaining the liver mass. Unfortunately, it also acts on stellate cells inducing a profibrogenic phenotype
机译:在非酒精性脂肪肝疾病(NAFLD)演变为脂肪性肝炎(NASH)的过程中,刺猬(Hh)通路最近与一种新的靶基因骨桥蛋白(OPN)有关,它是炎症和炎症协调的候选药物。纤维化发展。该途径在胚胎发生中至关重要,可以在组织再生的背景下在成年生活中激活。有研究表明,在脂毒性的背景下,垂死和受伤的肝细胞(如膨胀的肝细胞2)可产生Hh,然后Hh可作用于炎性细胞,例如天然杀伤性T(NKT)细胞和祖细胞。这样一种促进生长和肝细胞分化,维持肝脏肿块的方式。不幸的是,它也作用于星状细胞,诱导profibrogenic表型

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