ArticlePloS one2015
Cytoprotective Effect of Ferritin H in Renal Ischemia Reperfusion Injury.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Iron Biology in Acute Kidney Injury: Catalytic Iron, Hepcidin-Ferroportin Axis, and NGAL-A Narrative Review.International journal of molecular sciences · 2026Review
- Acute kidney injury and iron metabolism: A narrative review focusing on pathophysiology and therapy.Smart molecules : open access · 2025Review
- Ferroptotic mechanisms and therapeutic targeting of iron metabolism and lipid peroxidation in the kidney.Nature reviews. Nephrology · 2023Review
- Polyethylene glycol capped gold nanoparticles ameliorate renal ischemia-reperfusion injury in diabetic mice through AMPK-Nrf2 signaling pathway.Environmental science and pollution research international · 2022Article
- Heme Burden and Ensuing Mechanisms That Protect the Kidney: Insights from Bench and Bedside.International journal of molecular sciences · 2021Review
- Biochemistry of mammalian ferritins in the regulation of cellular iron homeostasis and oxidative responses.Science China. Life sciences · 2021Review
- Elevated serum iron level is a predictor of prognosis in ICU patients with acute kidney injury.BMC nephrology · 2020Article
- Air pollutants disrupt iron homeostasis to impact oxidant generation, biological effects, and tissue injury.Free radical biology & medicine · 2020Review
- Ferritins in Kidney Disease.Seminars in nephrology · 2020Review
- The multifaceted role of iron in renal health and disease.Nature reviews. Nephrology · 2020Review
- The Acute Phase Response Is a Prominent Renal Proteome Change in Sepsis in Mice.International journal of molecular sciences · 2019Article
- Article
- Ferritin in Kidney and Vascular Related Diseases: Novel Roles for an Old Player.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Article
- Programmed Necrosis and Disease:We interrupt your regular programming to bring you necroinflammation.Cell death and differentiation · 2019Review
- Acute and Chronic Iron Overloading Differentially Modulates the Expression of Cellular Iron-homeostatic Molecules in Normal Rat Kidney.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Article
- Farnesoid X receptor activation protects the kidney from ischemia-reperfusion damage.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress is a major contributor to kidney injury following ischemia reperfusion. Ferritin, a highly conserved iron-binding protein, is a key protein in the maintenance of cellular iron homeostasis and protection from oxidative stress. Ferritin mitigates oxidant stress by sequestering iron and preventing its participation in reactions that generate reactive oxygen species. Ferritin is composed of two subunit types, ferritin H and ferritin L. Using an in vivo model that enables conditional tissue-specific doxycycline-inducible expression of ferritin H in the mouse kidney, we tested the hypothesis that an increased level of H-rich ferritin is renoprotective in ischemic acute renal failure. Prior to induction of ischemia, doxycycline increased ferritin H in the kidneys of the transgenic mice nearly 6.5-fold. Following reperfusion for 24 hours, induction of neutrophil gelatinous-associated lipocalin (NGAL, a urine marker of renal dysfunction) was reduced in the ferritin H overexpressers compared to controls. Histopathologic examination following ischemia reperfusion revealed that ferritin H overexpression increased intact nuclei in renal tubules, reduced the frequency of tubular profiles with luminal cast materials, and reduced activated caspase-3 in the kidney. In addition, generation of 4-hydroxy 2-nonenal protein adducts, a measurement of oxidant stress, was decreased in ischemia-reperfused kidneys of ferritin H overexpressers. These studies demonstrate that ferritin H can inhibit apoptotic cell death, enhance tubular epithelial viability, and preserve renal function by limiting oxidative stress following ischemia reperfusion 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.