Section of Digestive Diseases, Yale University, New Haven, CT 06405, USA; West Haven VA, West Haven, CT 06516, USA.
Cell Metab. 2019 Jan 8;29(1):3-4. doi: 10.1016/j.cmet.2018.12.012.
Oxidative stress is uniformly present in non-alcoholic steatohepatitis (NASH), but its role in the development of liver inflammation and hepatocellular cancer (HCC) and the relationship between these two pathologies are poorly understood. In a recent issue of Cell, Grohmann et al. (2018) demonstrate a vital role of obesity-induced oxidative stress in deactivating the phosphatase TCPTP, resulting in activation of STAT-1 and STAT-3, which each independently drive the development of NASH and HCC, respectively.
氧化应激普遍存在于非酒精性脂肪性肝炎（NASH）中，但其在肝脏炎症和肝细胞癌（HCC）发展中的作用以及这两种病理之间的关系尚不清楚。在最近一期的《细胞》杂志上，Grohmann 等人（2018）证明了肥胖诱导的氧化应激在使磷酸酶 TCPTP 失活方面的重要作用，导致 STAT-1 和 STAT-3 的激活，它们分别独立地驱动 NASH 和 HCC 的发展。
