ArticleeLife2023
Iron status influences mitochondrial disease progression in Complex I-deficient mice.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 24 citations in OpenAlex.
- Moderate iron restriction improves metabolism via epigenetic regulation of GDF15.The Journal of nutritional biochemistry · 2026Article
- Targeting NDUFS4 Disrupts Oxidative Phosphorylation and Induces Ferroptosis in Olaparib-Resistant Prostate Cancer.Molecular cancer therapeutics · 2026Article
- Reimagining the contribution of iron in Parkinson's disease.Neurobiology of disease · 2026Review
- Interplay of anemia in inborn errors of energy metabolism.Scientific reports · 2026Observational
- Activation of PPARγ Attenuates Age-Related Lacrimal Gland Dysfunction by Alleviating Endoplasmic Reticulum Stress-Mediated Ferroptosis.Investigative ophthalmology & visual science · 2026Article
- Beyond the Brain: Exploring the multi-organ axes in Parkinson's disease pathogenesis.Journal of advanced research · 2026Review
- Elevated maternal pre-transfer serum lipid peroxidation is associated with implantation failure and early pregnancy loss.BMC medicine · 2026Article
- Metal Ions Within the Neuro-Immune-Tumor Axis.Journal of immunology research · 2026Review
- Multiplexed quantum sensing reveals coordinated thermomagnetic regulation of mitochondria.bioRxiv : the preprint server for biology · 2025Article
- Inhibition of Ferroptosis Delays Aging and Extends Healthspan Across Multiple Species.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Selenoprotein K Confers Protection against Iron Dyshomeostasis-Related Neurotoxicity by Regulating the Palmitoylation of TfR-1.Journal of agricultural and food chemistry · 2025Article
- Mitochondrial translation regulates terminal erythroid differentiation by maintaining iron homeostasis.Science advances · 2025Article
- Peripheral Blood Immune Cells from Individuals with Parkinson's Disease or Inflammatory Bowel Disease Share Deficits in Iron Storage and Transport that are Modulated by Non-Steroidal Anti-Inflammatory Drugs.bioRxiv : the preprint server for biology · 2024Article
- Modulation of calcium signaling and metabolic pathways in endothelial cells with magnetic fields.Nanoscale advances · 2024Article
- Defective function of α-ketoglutarate dehydrogenase exacerbates mitochondrial ATP deficits during complex I deficiency.Redox biology · 2023Article
- Role of liensinine in sensitivity of activated macrophages to ferroptosis and in acute liver injury.Cell death discovery · 2023Article
- Article
- Understanding Long COVID; Mitochondrial Health and Adaptation-Old Pathways, New Problems.Biomedicines · 2022Review
- Mitochondrial CytochromeFrontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction caused by aberrant Complex I assembly and reduced activity of the electron transport chain is pathogenic in many genetic and age-related diseases. Mice missing the Complex I subunit NADH dehydrogenase [ubiquinone] iron-sulfur protein 4 (NDUFS4) are a leading mammalian model of severe mitochondrial disease that exhibit many characteristic symptoms of Leigh Syndrome including oxidative stress, neuroinflammation, brain lesions, and premature death. NDUFS4 knockout mice have decreased expression of nearly every Complex I subunit. As Complex I normally contains at least 8 iron-sulfur clusters and more than 25 iron atoms, we asked whether a deficiency of Complex I may lead to iron perturbations, thereby accelerating disease progression. Consistent with this, iron supplementation accelerates symptoms of brain degeneration in these mice, while iron restriction delays the onset of these symptoms, reduces neuroinflammation, and increases survival. NDUFS4 knockout mice display signs of iron overload in the liver including increased expression of hepcidin and show changes in iron-responsive element-regulated proteins consistent with increased cellular iron that were prevented by iron restriction. These results suggest that perturbed iron homeostasis may contribute to pathology in Leigh Syndrome and possibly other mitochondrial disorders.
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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.