ArticleFree radical biology & medicine2021
Iron deficiency exacerbates cisplatin- or rhabdomyolysis-induced acute kidney injury through promoting iron-catalyzed oxidative damage.
Article in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Effect of Intravenous Iron Dextran on Kidney Outcomes in Acute Kidney Injury with Iron Deficiency: A Randomized Trial.Kidney360 · 2026Trial
- Impact of hemoglobin increase in patients with acute kidney injury and severe anemia on major adverse kidney events.Renal failure · 2026Article
- Review
- Ionizing radiation promotes lung injury by inducing ferroptosis-driven senescence in epithelial cells via NCOA4-mediated ferritinophagy.Redox biology · 2026Article
- Iron deficiency anemia is associated with renal function decline in obstructive sleep apnea: a multi-institutional cohort study.Frontiers in nutrition · 2026Article
- Pre-existing iron deficiency anemia and long-term risk of recurrent acute kidney injury in survivors of ICU-associated AKI: a propensity-matched study.Frontiers in nutrition · 2026Article
- Ferroptosis in Cancer and Inflammatory Diseases: Mechanisms and Therapeutic Implications.MedComm · 2025Review
- Salvianolic Acid B Attenuates Ferroptosis in Acute Kidney Injury by Targeting PRDX5.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The role of ferroptosis in acute kidney injury: mechanisms and potential therapeutic targets.Molecular and cellular biochemistry · 2025Review
- Review
- Hazel Leaf Polyphenol Extract Alleviated Cisplatin-Induced Acute Kidney Injury by Reducing Ferroptosis through Inhibiting Hippo Signaling.Molecules (Basel, Switzerland) · 2024Article
- Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities.Frontiers in immunology · 2024Review
- Emerging significance and therapeutic targets of ferroptosis: a potential avenue for human kidney diseases.Cell death & disease · 2023Review
- Article
- Paricalcitol Ameliorates Acute Kidney Injury in Mice by Suppressing Oxidative Stress and Inflammation via Nrf2/HO-1 Signaling.International journal of molecular sciences · 2023Article
- Molecular Mechanisms of Ferroptosis and Their Involvement in Acute Kidney Injury.Journal of inflammation research · 2023Review
- Farnesoid X receptor protects against cisplatin-induced acute kidney injury by regulating the transcription of ferroptosis-related genes.Redox biology · 2022Article
- Ferroptosis and its role in skeletal muscle diseases.Frontiers in molecular biosciences · 2022Review
- Preparation, structural characterization, antioxidant activity and protection against cisplatin-induced acute kidney injury by polysaccharides from the lateral root of Aconitum carmichaelii.Frontiers in pharmacology · 2022Article
- Functional consequence of myeloid ferritin heavy chain on acute and chronic effects of rhabdomyolysis-induced kidney injury.Frontiers in medicine · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
Iron deficiency is the most common micronutrient deficiency worldwide. While iron deficiency is known to suppress embryonic organogenesis, its effect on the adult organ in the context of clinically relevant damage has not been considered. Here we report that iron deficiency is a risk factor for nephrotoxic intrinsic acute kidney injury of the nephron (iAKI). Iron deficiency exacerbated cisplatin-induced iAKI by markedly increasing non-heme catalytic iron and Nox4 protein which together catalyze production of hydroxyl radicals followed by protein and DNA oxidation, apoptosis and ferroptosis. Crosstalk between non-heme catalytic iron/Nox4 and downstream oxidative damage generated a mutual amplification cycle that facilitated rapid progression of cisplatin-induced iAKI. Iron deficiency also exacerbated a second model of iAKI, rhabdomyolysis, via increasing catalytic heme-iron. Heme-iron induced lipid peroxidation and DNA oxidation by interacting with Nox4-independent mechanisms, promoting p53/p21 activity and cellular senescence. Our data suggests that correcting iron deficiency and/or targeting specific catalytic iron species are strategies to mitigate iAKI in a wide range of patients with diverse forms of kidney injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.