Division of Science and Engineering, Penn State University, Abington College, Abington, PA 19001, USA.
Iowa City Veterans Administration Medical Center, Iowa City, IA 52242, USA.
Int J Mol Sci. 2019 Apr 30;20(9):2132. doi: 10.3390/ijms20092132.
Iron is implicated in the pathogenesis of a number of human liver diseases. Hereditary hemochromatosis is the classical example of a liver disease caused by iron, but iron is commonly believed to contribute to the progression of other forms of chronic liver disease such as hepatitis C infection and nonalcoholic fatty liver disease. In this review, we present data from cell culture experiments, animal models, and clinical studies that address the hepatotoxicity of iron. These data demonstrate that iron overload is only weakly fibrogenic in animal models and rarely causes serious liver damage in humans, calling into question the concept that iron overload is an important cause of hepatotoxicity. In situations where iron is pathogenic, iron-induced liver damage may be potentiated by coexisting inflammation, with the resulting hepatocyte necrosis an important factor driving the fibrogenic response. Based on the foregoing evidence that iron is less hepatotoxic than is generally assumed, claims that assign a causal role to iron in liver injury in either animal models or human liver disease should be carefully evaluated.
铁元素与许多人类肝脏疾病的发病机制有关。遗传性血色素沉着症是由铁引起的典型肝脏疾病,但人们普遍认为铁会促进其他类型慢性肝脏疾病(如丙型肝炎感染和非酒精性脂肪性肝病)的进展。在这篇综述中,我们呈现了来自细胞培养实验、动物模型和临床研究的数据,这些数据涉及铁的肝毒性。这些数据表明,铁过载在动物模型中仅有微弱的致纤维化作用,并且在人类中很少导致严重的肝脏损伤,这使得铁过载是肝毒性的一个重要原因这一概念受到质疑。在铁致病的情况下,铁诱导的肝损伤可能会被共存的炎症增强,由此导致的肝细胞坏死是驱动纤维化反应的一个重要因素。基于铁的肝毒性比一般认为的要低这一证据,在动物模型或人类肝脏疾病中,将铁与肝损伤联系起来的说法应该被仔细评估。