ArticleJournal of the American Society of Nephrology : JASN2015
Hepcidin Mitigates Renal Ischemia-Reperfusion Injury by Modulating Systemic Iron Homeostasis.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- Iron metabolism-related indicators as predictors of the incidence of acute kidney injury after cardiac surgery: a meta-analysis.Renal failure · 2023Pooled it
- Silencing of HAVCR2 Attenuates Skeletal Muscle Ischemia-Reperfusion Injury by Inhibiting Oxidative Stress.Biochemical genetics · 2026Article
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Iron Biology in Acute Kidney Injury: Catalytic Iron, Hepcidin-Ferroportin Axis, and NGAL-A Narrative Review.International journal of molecular sciences · 2026Review
- Selenoprotein GPX3 regulates NADPH oxidase expression by inhibiting the MAPK signaling pathway and thereby attenuating the inflammatory response in renal ischemia-reperfusion injury.Genes & diseases · 2026Article
- Acute kidney injury and iron metabolism: A narrative review focusing on pathophysiology and therapy.Smart molecules : open access · 2025Review
- Iron-related protein in prediction of acute kidney injury in the pediatric population after cardiac surgery.Journal of cardiothoracic surgery · 2025Article
- [Inhibition of ferroptosis alleviates acute kidney injury caused by diquat in zebrafish].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Effects of Peptides and Bioactive Peptides on Acute Kidney Injury: A Review Study.Iranian biomedical journal · 2025Review
- Progression of Kidney Fibrosis after Sepsis: Underestimated Role of Resident Macrophages and Recruited Monocytes.Journal of the American Society of Nephrology : JASN · 2025Review
- The role of ferroptosis in acute kidney injury: mechanisms and potential therapeutic targets.Molecular and cellular biochemistry · 2025Review
- Development and Validation of a Diagnostic Model for AKI Based on the Analysis of Ferroptosis-related Genes.Current medicinal chemistry · 2025Article
- Role of Iron Metabolic Disturbances and Inflammatory Iron Biomarkers in Liver Transplant Prognosis.International journal of medical sciences · 2025Review
- Article
- Iron as an emerging therapeutic target in critically ill patients.Critical care (London, England) · 2023Review
- Iron metabolism and chronic inflammation in IgA nephropathy.Renal failure · 2023Review
- Male kidney-specific BMAL1 knockout mice are protected from KAmerican journal of physiology. Renal physiology · 2023Article
- Attenuation of Sepsis-Induced Acute Kidney Injury by Exogenous HMolecules (Basel, Switzerland) · 2023Article
- Ferroptosis: From regulation of lipid peroxidation to the treatment of diseases.Cell biology and toxicology · 2023Review
- Regulated cell death pathways in kidney disease.Nature reviews. Nephrology · 2023Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron-mediated oxidative stress is implicated in the pathogenesis of renal ischemia-reperfusion injury. Hepcidin is an endogenous acute phase hepatic hormone that prevents iron export from cells by inducing degradation of the only known iron export protein, ferroportin. In this study, we used a mouse model to investigate the effect of renal ischemia-reperfusion injury on systemic iron homeostasis and determine if dynamic modulation of iron homeostasis with hepcidin has therapeutic benefit in the treatment of AKI. Renal ischemia-reperfusion injury induced hepatosplenic iron export through increased ferroportin expression, which resulted in hepatosplenic iron depletion and an increase in serum and kidney nonheme iron levels. Exogenous hepcidin treatment prevented renal ischemia-reperfusion-induced changes in iron homeostasis. Hepcidin also decreased kidney ferroportin expression and increased the expression of cytoprotective H-ferritin. Hepcidin-induced restoration of iron homeostasis was accompanied by a significant reduction in ischemia-reperfusion-induced tubular injury, apoptosis, renal oxidative stress, and inflammatory cell infiltration. Hepcidin -: deficient mice demonstrated increased susceptibility to ischemia-reperfusion injury compared with wild-type mice. Reconstituting hepcidin-deficient mice with exogenous hepcidin induced hepatic iron sequestration, attenuated the reduction in renal H-ferritin and reduced renal oxidative stress, apoptosis, inflammation, and tubular injury. Hepcidin-mediated protection was associated with reduced serum IL-6 levels. In summary, renal ischemia-reperfusion injury results in profound alterations in systemic iron homeostasis. Hepcidin treatment restores iron homeostasis and reduces inflammation to mediate protection in renal ischemia-reperfusion injury, suggesting that hepcidin-ferroportin pathway holds promise as a novel therapeutic target in the treatment of AKI.
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