In the process of mammalian life ,it is almost inseparable from the redox properties of copper and iron . Copper is often used as a complementary group in the form of Cu +that associated with some related proteins ,and the structures of copper-binding proteins play important roles in their biological function .The kidney is the organ of copper excretion .The absorption ,storage ,release ,and transport of copper in the kidney cells are important for copper homeostasis in the kidney .The imbalance of copper homeostasis in the kidneys causes disruption of the mi-tochondrial structure in the kidneys ,and the loss of renal cells leads to impaired renal excretion .With the study of the renal copper transporter and the target cells .this article reviewed the intracellular binding pathways of mito-chondria ,Golgi ,and cytoplasm with copper chaperones and copper transporters ,clarified the mechanism of copper transporter (CTR1) expression and the mechanism of redistribution of protein (ATP7A) and protein (ATP7B) under the high level of copper in order to reveal the theoretical basis of the renal copper homeostasis mechanism .%哺乳动物的生命活动过程中,几乎离不开铜和铁的氧化还原特性反应,并且铜常以Cu2+的形式与其相关蛋白结合的形式作为一些功能性蛋白的辅基,同时铜结合蛋白的结构在其发挥生物学功能过程中具有重要作用.肾脏是铜排泄的器官,肾脏细胞内铜的吸收、储存、释放、转运对肾脏铜稳态很重要,肾脏铜稳态的失衡使肾脏线粒体结构发生断裂,肾脏细胞脱落导致肾脏排泄发生障碍.随着对肾脏铜转运因子与靶细胞器研究的逐步深入,论文综述了胞内的线粒体、高尔基体、胞浆分别与铜伴侣蛋白、铜转运蛋白的结合途径,阐明了铜转运蛋白(CTR1)的表达机制,铜离子转出蛋白(ATP7A)、铜离子转出蛋白(ATP7B)在高铜情况下的再分配机制,为揭示肾脏铜稳态机制奠定理论基础.
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