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首页> 外文期刊>American Journal of Physiology >Physiology of iron transport and the hemochromatosis gene.
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Physiology of iron transport and the hemochromatosis gene.

机译：铁转运的生理和血色素沉着病基因。

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Iron is essential for fundamental cell functions but is also a catalyst for chemical reactions involving free radical formation, potentially leading to oxidative stress and cell damage. Cellular iron levels are therefore carefully regulated to maintain an adequate substrate while also minimizing the pool of potentially toxic "free iron." The main control of body iron homeostasis in higher organisms is placed in the duodenum, where dietary iron is absorbed, whereas no controlled means of eliminating unwanted iron have evolved in mammals. Hereditary hemochromatosis, the prototype of deregulated iron homeostasis in humans, is due to inappropriately increased iron absorption and is commonly associated to a mutated HFE gene. The HFE protein is homologous to major histocompatibility complex class I proteins but is not an iron carrier, whereas biochemical and cell biological studies have shown that the transferrin receptor, the main protein devoted to cellular uptake of transferrin iron, interacts with HFE. This review focuses on recent advances in iron research and presents a model of HFE function in iron metabolism.
机译：铁对细胞的基本功能至关重要，但它也是涉及自由基形成的化学反应的催化剂，可能导致氧化应激和细胞损伤。因此，细胞铁的水平要经过仔细调节，以维持足够的底物，同时也将潜在的有毒“游离铁”的含量降至最低。在高等生物体中，体内铁稳态的主要控制位于十二指肠，在那里吸收膳食中的铁，而在哺乳动物中尚未形成消除有害铁的受控方法。遗传性血色素沉着症是人类体内铁稳态失调的原型，是由于铁吸收不适当增加，通常与HFE基因突变有关。 HFE蛋白与主要的组织相容性复合体I类蛋白同源，但不是铁载体，而生化和细胞生物学研究表明，转铁蛋白受体是致力于细胞摄取转铁蛋白铁的主要蛋白，它与HFE相互作用。这篇综述着重于铁研究的最新进展，并提出了HFE在铁代谢中的功能模型。

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