中文摘要：

铁调素（Hepcidin）是由肝细胞分泌的维持人体系统性铁平衡的核心因子，其通过改变细胞膜铁转运蛋白（ferroportin，Fpn）的表达量以调控肠黏膜细胞和巨噬细胞内铁的转出水平，从而决定机体循环铁水平并影响肝脏等主要储铁脏器的铁负荷程度。根据近年来的研究发现，影响Hepcidin表达的主要因素可以归纳为两个方面：一是机体本身对铁的需求，而由于铁本身又是Hb（hemoglobin，血红蛋白）的合成原料以及携氧成份，因此还应包括机体对Hb合成和缺氧的反应，介导因子主要包括携铁转铁蛋白（holo—transferrin，holo—Tf）、促红细胞生成素（erythropoietin，EPO）和缺氧诱导因子-1（hypoxia．inducible factor1，HIF．1）；另一则是源于疾病病理过程中相关致病因素、细胞因子、激素等非铁调控因子的改变对其表达调控机制产生的影响，并通过扰乱机体铁稳态加速疾病的发展或加重病情。随着研究资料的积累，糖尿病、部分心血管疾病、酒精性或非酒精性脂肪肝等慢性疾病存在铁过负荷已是不争的事实，多种hepcidin非铁调控因子在代谢紊乱型铁过负荷综合征（sysmetabolic iron overload syndrome）发生过程中的作用受到了广泛重视。对一些常见疾病中引起hepcidin表达变化异常和铁代谢紊乱的非铁因子及其作用机制的研究进展进行综述。

英文摘要：

Hepcidin, which is secreted by the hepatocyte, is a core factor to maintain the systemic iron balance by regulating the iron output of intestinal mucosal cells and macrophages through changing the ferroportin expression on the cell membrane. Thus, the expression of hepcidin can significantly affect the extent of iron load of the major iron storage organs like liver by deciding the body circulating iron levels. Recent studies show that the main factors affecting the hepcidin expression can be summarized into two aspects, one is the body demand for iron, includingHb （hemoglobin） synthesis and the hypoxic response because iron itself is synthetic materials as well as oxygencarrying component of the Hb, which contain holo-Tf （holo-transferrin）, EPO （erythropoietin） and HIF-1 （hypoxiainducible factor 1）; the other is the disease-related factors like cytokines, hormones and other non-iron regulatory factors, most of which play a key role in the pathophysiological process and may accelerate the development of the disease by disrupting the body iron homeostasis. With the accumulation of research data, it is considered as an indisputable fact that some cardiovascular disease, diabetes, alcohol or non-alcoholic fatty liver disease and other chronic diseases exists iron overload, extensive attention have been paid to the role of a variety of hepcidin non-iron regulatory factors in the sysmetabolic iron overload syndrome. This article will review the non-iron regulators and its mechanisms to cause the abnormal expression ofhepcidin and iron overload in some common diseases.