ReviewAntioxidants (Basel, Switzerland)2023
Dysregulated Iron Homeostasis as Common Disease Etiology and Promising Therapeutic Target.
Review in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Approach to anaemia in gastrointestinal disease: A position paper by the ESPGHAN Gastroenterology Committee.Journal of pediatric gastroenterology and nutrition · 2025Guideline
- Iron Homeostasis and Reproduction: Unveiling the Microbiome-Gut-Brain Axis Connection in the MosquitoCells · 2026Article
- Mechanism of Ferroptosis in Cardiovascular Disease and Its Regulation by Natural Compounds: A Narrative Review.Drug design, development and therapy · 2026Review
- Targeting Aging and Diseases Associated with Ferroptosis and Senescence Through Modulation of Iron, Oxidative Stress and Lipid Peroxidation.Antioxidants (Basel, Switzerland) · 2025Review
- Pharmacological and toxicological insights into the ayurvedic formulation Rasasindura.Scientific reports · 2025Article
- Study on anti-fatigue effect and mechanism of iron source combined with Angelica sinensis and Agrimonia pilosa on pigeons under exercise stress.Poultry science · 2025Article
- Akkermansia muciniphila MucNature communications · 2025Article
- Review
- The Causal Effect of Iron Traits on Risk of Hypertrophic Scarring: A Two-Sample Mendelian Randomization Study.Journal of cosmetic dermatology · 2025Article
- The interplay of iron, oxidative stress, and α-synuclein in Parkinson's disease progression.Molecular medicine (Cambridge, Mass.) · 2025Review
- Ferroptosis-Related Genes as Molecular Markers in Bovine Mammary Epithelial Cells Challenged withInternational journal of molecular sciences · 2025Article
- The Multifaceted Role of Macrophages in Biology and Diseases.International journal of molecular sciences · 2025Review
- Iron Homeostasis Dysregulation, Oro-Gastrointestinal Microbial Inflammatory Factors, and Alzheimer's Disease: A Narrative Review.Microorganisms · 2025Review
- Oxidative Stress: A New Pathophysiological Pathway in Parkinson's Disease and a Potential Target of the Brain-Sport Crosstalk.Parkinson's disease · 2025Review
- Traditional Chinese Medicine and Ferroptosis in Intracerebral Hemorrhage: A Potential Therapeutic Approach.Drug design, development and therapy · 2025Review
- Effects of Iron, Copper, Zinc, and Magnesium on Chronic Widespread Pain: A Two-Sample Mendelian Randomization.Journal of clinical medicine · 2024Article
- Meconium Proteins Involved in Iron Metabolism.International journal of molecular sciences · 2024Article
- PARP14 Contributes to the Development of the Tumor-Associated Macrophage Phenotype.International journal of molecular sciences · 2024Article
- Interplay of Ferroptosis and Cuproptosis in Cancer: Dissecting Metal-Driven Mechanisms for Therapeutic Potentials.Cancers · 2024Review
- Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective.Frontiers in neurology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron is irreplaceably required for animal and human cells as it provides the activity center for a wide variety of essential enzymes needed for energy production, nucleic acid synthesis, carbon metabolism and cellular defense. However, iron is toxic when present in excess and its uptake and storage must, therefore, be tightly regulated to avoid damage. A growing body of evidence indicates that iron dysregulation leading to excess quantities of free reactive iron is responsible for a wide range of otherwise discrete diseases. Iron excess can promote proliferative diseases such as infections and cancer by supplying iron to pathogens or cancer cells. Toxicity from reactive iron plays roles in the pathogenesis of various metabolic, neurological and inflammatory diseases. Interestingly, a common underlying aspect of these conditions is availability of excess reactive iron. This underpinning aspect provides a potential new therapeutic avenue. Existing hematologically used iron chelators to take up excess iron have shown serious limitations for use but new purpose-designed chelators in development show promise for suppressing microbial pathogen and cancer cell growth, and also for relieving iron-induced toxicity in neurological and other diseases. Hepcidin and hepcidin agonists are also showing promise for relieving iron dysregulation. Harnessing iron-driven reactive oxygen species (ROS) generation with ferroptosis has shown promise for selective destruction of cancer cells. We review biological iron requirements, iron regulation and the nature of iron dysregulation in various diseases. Current results pertaining to potential new therapies are also reviewed.
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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.