Role of Endoplasmic Reticulum Stress in Drug-Induced Liver Disease

我们去年报道了氟烷代谢导致未折叠蛋白反应（UPR）和随后的肝损伤，其部分原因似乎是由于缺乏蛋白质合成的蛋白质分解代谢导致肝脏中重要抗氧化蛋白的损失。今年，我们采用了一种公正的全球蛋白质组学方法来鉴定氟烷治疗后肝脏中丢失的其他肝保护蛋白。

We reported last year that halothane metabolism led to an unfolded protein response (UPR) and subsequent liver injury that appeared to be due in part to a loss of important antioxidant proteins from the liver as a result of protein catabolism in the absence of protein synthesis. This year we have taken an unbiased global proteomics approach to identify other hepatoprotective proteins that are lost from liver following halothane treatment. Conclusion: The murine model of halothane-induced liver injury continues to reveal novel mechanisms of DILD. Our proteomics findings this year suggest that the UPR and turnover of numerous other hepatoprotective proteins may also contribute to the hepatotoxic potential of not only halothane, but also of other drugs that induce the UPR.