首页> 外文期刊>Journal of Pathology: Journal of the Pathological Society of Great Britain and Ireland >New wine into old wineskins: PGC‐1α and NF‐κB in obesity and acute pancreatitis
【24h】

New wine into old wineskins: PGC‐1α and NF‐κB in obesity and acute pancreatitis

机译:新葡萄酒变成旧葡萄干:PGC-1α和NF-κB在肥胖症和急性胰腺炎中

获取原文
获取原文并翻译 | 示例
           

摘要

Abstract Obesity and acute pancreatitis are both proinflammatory conditions. Importantly, obesity increases severity in acute pancreatitis by enhancing inflammation. In a recent issue of The Journal of Pathology , Pérez and Ruiz‐Pérez et al connected obesity and pancreatitis for the first time, through the transcriptional regulator PPARγ coactivator 1α (PGC‐1α). Obesity reduces pancreatic PGC‐1α levels and potentiates not only oxidative but also IL‐6‐mediated inflammatory damage during acute pancreatitis by relieving the binding of PGC‐1α to the NF‐κB subunit p65. Blockade of the IL‐6 receptor subunit gp130 ameliorated tissue injury, substantiating the importance of deregulated PGC‐1α/p65/IL‐6 signaling in obesity and acute pancreatitis. Copyright ? 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
机译:摘要肥胖和急性胰腺炎都是促炎症的条件。 重要的是,肥胖通过增强炎症来增加急性胰腺炎的严重程度。 在最近的病理学,Pérez和Ruiz-Pérez等,首次通过转录调节剂PPARγ共催粘剂1α(PGC-1α)连接肥胖症和胰腺炎。 肥胖症通过将PGC-1α与NF-κB亚基P65的结合减少,降低了胰腺PGC-1α水平,并且增强剂不仅氧化,而且在急性胰腺炎中介导的IL-6介导的炎症损伤。 IL-6受体亚基GP130改善组织损伤的阻断,证实了DEERUPATION PGC-1α/ P65 / IL-6在肥胖症和急性胰腺炎中的重要性。 版权? 2018年大英国和爱尔兰病理学协会。 John Wiley&amp出版; SONS,LTD.

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