海西定
铁转运蛋白
重吸收
平衡
肾
内分泌学
内科学
化学
缺铁
医学
贫血
作者
Allison L. Fisher,Jodie L. Babitt
标识
DOI:10.1016/j.kint.2021.06.023
摘要
Iron balance is tightly controlled to provide adequate amounts of this essential nutrient, but to limit the adverse effects of excess iron. Key mediators of systemic iron homeostasis are the iron regulatory hormone hepcidin and its receptor, the iron export protein ferroportin. A new study by Mohammad et al. demonstrates the functional role of the hepcidin-ferroportin axis in the kidney, and how this contributes to kidney iron levels and the systemic iron economy. Iron balance is tightly controlled to provide adequate amounts of this essential nutrient, but to limit the adverse effects of excess iron. Key mediators of systemic iron homeostasis are the iron regulatory hormone hepcidin and its receptor, the iron export protein ferroportin. A new study by Mohammad et al. demonstrates the functional role of the hepcidin-ferroportin axis in the kidney, and how this contributes to kidney iron levels and the systemic iron economy. The kidney hepcidin/ferroportin axis controls iron reabsorption and determines the magnitude of kidney and systemic iron overloadKidney InternationalVol. 100Issue 3PreviewThe hepcidin/ferroportin axis controls systemic iron homeostasis by regulating iron acquisition from the duodenum and reticuloendothelial system, respective sites of iron absorption and recycling. Ferroportin is also abundant in the kidney, where it has been implicated in tubular iron reabsorption. However, it remains unknown whether endogenous hepcidin regulates ferroportin-mediated iron reabsorption under physiological conditions, and whether such regulation is important for kidney and/or systemic iron homeostasis. Full-Text PDF Open Access
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