ArticleKidney international2021
The kidney hepcidin/ferroportin axis controls iron reabsorption and determines the magnitude of kidney and systemic iron overload.
Article in Kidney international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 33 citations in OpenAlex.
- Mitochondrial dysfunction-ferroptosis crosstalk drives renal fibrosis in chronic kidney disease.Renal failure · 2026Review
- The crosstalk between iron metabolism and immune tolerance in autoimmunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Endothelin receptor antagonism in sickle cell disease: Is the time now?Canadian journal of physiology and pharmacology · 2026Review
- Article
- Research progress of traditional Chinese medicines in regulating acute kidney injury-related ferroptosis: a literature review.International urology and nephrology · 2025Review
- Article
- Risk factors for hemorrhagic cystitis in children with severe beta-thalassemia after allogeneic hematopoietic stem cell transplantation.Frontiers in pediatrics · 2025Article
- Therapeutic targeting of the hepcidin-ferroportin axis and erythropoietic modulators: a narrative review.Frontiers in medicine · 2025Review
- Artesunate alleviates kidney fibrosis by restoring klotho protein and suppressing Wnt/β-catenin signalling pathway.Frontiers in cell and developmental biology · 2025Article
- Iron deficiency and supplementation in heart failure.Nature reviews. Cardiology · 2024Review
- Advances of Iron and Ferroptosis in Diabetic Kidney Disease.Kidney international reports · 2024Review
- Iron Metabolism and Inflammatory Mediators in Patients with Renal Dysfunction.International journal of molecular sciences · 2024Review
- Mechanisms controlling cellular and systemic iron homeostasis.Nature reviews. Molecular cell biology · 2024Review
- Renal-specific loss of ferroportin disrupts iron homeostasis and attenuates recovery from acute kidney injury.American journal of physiology. Renal physiology · 2024Article
- Iron metabolism and chronic inflammation in IgA nephropathy.Renal failure · 2023Review
- Animal models of kidney iron overload and ferroptosis: a review of the literature.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Review
- The mechanism of ferroptosis and its related diseases.Molecular biomedicine · 2023Review
- Induction of Hepcidin Expression in the Renal Cortex of Sickle Cell Disease Mice.International journal of molecular sciences · 2023Article
- Distinctive modulation of hepcidin in cancer and its therapeutic relevance.Frontiers in oncology · 2023Review
- Capsaicin Decreases Kidney Iron Deposits and Increases Hepcidin Levels in Diabetic Rats with Iron Overload: A Preliminary Study.Molecules (Basel, Switzerland) · 2022Article
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Abstract
The 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. To address these questions, we generated a novel mouse model with an inducible kidney-tubule specific knock-in of fpnC326Y, which encodes a hepcidin-resistant ferroportin termed FPNC326Y. Under conditions of normal iron availability, female mice harboring this allele had consistently decreased kidney iron but only transiently increased systemic iron indices. Under conditions of excess iron availability, male and female mice harboring this allele had milder kidney iron overload, but greater systemic iron overload relative to controls. Additionally, despite comparable systemic iron overload, kidney iron overload occurred in wild type mice fed an iron-loaded diet but not in hemochromatosis mice harboring a ubiquitous knock-in of fpnC326Y. Thus, our study demonstrates that endogenous hepcidin controls ferroportin-mediated tubular iron reabsorption under physiological conditions. It also shows that such control is important for both kidney and systemic iron homeostasis in the context of iron overload.
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