The Role of Iron and Iron Overload in Chronic Liver Disease.
The Role of Iron and Iron Overload in Chronic Liver Disease.
复制标题
DOI：
10.12659/msm.896494
复制
发表时间：
2016-06-22
期刊：
影响因子：
--
通讯作者：
Ristic S
中科院分区：
文献类型：
--
作者：
Milic S;Mikolasevic I;Orlic L;Devcic E;Starcevic-Cizmarevic N;Stimac D;Kapovic M;Ristic S
肝脏在铁稳态中发挥着重要作用。因此，慢性肝病患者的铁调节可能会受到干扰。较高的铁水平不仅存在于遗传性血色素沉着病患者中，而且存在于酒精性肝病、非酒精性脂肪肝病和丙型肝炎病毒感染患者中。慢性肝病会降低肝脏的合成功能，包括铁调素（铁代谢中的关键蛋白质）的产生。铁调素水平较低会导致铁超载，从而导致肝脏中铁沉积和血液中非转铁蛋白结合铁水平升高。铁与活性氧结合会导致羟基自由基增加，从而导致磷脂过氧化、氨基酸侧链氧化、DNA 应变断裂和蛋白质断裂。铁诱导的细胞损伤可以通过调节铁调素的产生或施用铁调素激动剂来预防。这两种方法都在小鼠模型中取得了成功的结果。
The liver plays a major role in iron homeostasis; thus, in patients with chronic liver disease, iron regulation may be disturbed. Higher iron levels are present not only in patients with hereditary hemochromatosis, but also in those with alcoholic liver disease, nonalcoholic fatty liver disease, and hepatitis C viral infection. Chronic liver disease decreases the synthetic functions of the liver, including the production of hepcidin, a key protein in iron metabolism. Lower levels of hepcidin result in iron overload, which leads to iron deposits in the liver and higher levels of non-transferrin-bound iron in the bloodstream. Iron combined with reactive oxygen species leads to an increase in hydroxyl radicals, which are responsible for phospholipid peroxidation, oxidation of amino acid side chains, DNA strain breaks, and protein fragmentation. Iron-induced cellular damage may be prevented by regulating the production of hepcidin or by administering hepcidin agonists. Both of these methods have yielded successful results in mouse models.