ArticleThe American journal of pathology2019
Liver-Specific, but Not Retina-Specific, Hepcidin Knockout Causes Retinal Iron Accumulation and Degeneration.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
20 citing papers in PubMed, 29 citations in OpenAlex.
- A large cohort analysis of metabolic signatures underlying the liver-eye axis.Communications medicine · 2026Article
- Oral Deuterated Docosahexaenoic Acid Protects Against Onset and Progression of RPE Degeneration in a Mouse Model of Chronic Oxidative Stress.Investigative ophthalmology & visual science · 2026Article
- Article
- Testosterone promotes photoreceptor degeneration in the sodium iodate model.Experimental eye research · 2025Article
- Photoreceptor metabolic window unveils eye-body interactions.Nature communications · 2025Article
- Identification of Ferroptosis-Related Gene in Age-Related Macular Degeneration Using Machine Learning.Immunity, inflammation and disease · 2024Article
- Insights into the liver-eyes connections, from epidemiological, mechanical studies to clinical translation.Journal of translational medicine · 2023Review
- Low ceruloplasmin levels exacerbate retinal degeneration in a hereditary hemochromatosis model.Disease models & mechanisms · 2023Article
- Oxidative stress induces lysosomal membrane permeabilization and ceramide accumulation in retinal pigment epithelial cells.Disease models & mechanisms · 2023Article
- Cytochrome P450 1B1 Expression Regulates Intracellular Iron Levels and Oxidative Stress in the Retinal Endothelium.International journal of molecular sciences · 2023Article
- Engineering siderophore production in Pseudomonas to improve asbestos weathering.Microbial biotechnology · 2022Article
- Retina tissue validation of optical coherence tomography determined outer nuclear layer loss in FTLD-tau.Acta neuropathologica communications · 2021Article
- Bisretinoids of the Retina: Photo-Oxidation, Iron-Catalyzed Oxidation, and Disease Consequences.Antioxidants (Basel, Switzerland) · 2021Review
- Beyond the Liver: Liver-Eye Communication in Clinical and Experimental Aspects.Frontiers in molecular biosciences · 2021Review
- Effects of Excess Iron on the Retina: Insights From Clinical Cases and Animal Models of Iron Disorders.Frontiers in neuroscience · 2021Review
- Ferrous but not ferric iron sulfate kills photoreceptors and induces photoreceptor-dependent RPE autofluorescence.Redox biology · 2020Article
- Review
- Local synthesis of hepcidin in the anterior segment of the eye: A novel observation with physiological and pathological implications.Experimental eye research · 2020Article
- Iron Accumulates in Retinal Vascular Endothelial Cells But Has Minimal Retinal Penetration After IP Iron Dextran Injection in Mice.Investigative ophthalmology & visual science · 2019Article
- A vicious cycle of bisretinoid formation and oxidation relevant to recessive Stargardt disease.The Journal of biological chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
Abstract
The liver secretes hepcidin (Hepc) into the bloodstream to reduce blood iron levels. Hepc accomplishes this by triggering degradation of the only known cellular iron exporter ferroportin in the gut, macrophages, and liver. We previously demonstrated that systemic Hepc knockout (HepcKO) mice, which have high serum iron, develop retinal iron overload and degeneration. However, it was unclear whether this is caused by high blood iron levels or, alternatively, retinal iron influx that would normally be regulated by retina-produced Hepc. To address this question, retinas of liver-specific and retina-specific HepcKO mice were studied. Liver-specific HepcKO mice had elevated blood and retinal pigment epithelium (RPE) iron levels and increased free (labile) iron levels in the retina, despite an intact blood-retinal barrier. This led to RPE hypertrophy associated with lipofuscin-laden lysosome accumulation. Photoreceptors also degenerated focally. In contrast, there was no change in retinal or RPE iron levels or degeneration in the retina-specific HepcKO mice. These data indicate that high blood iron levels can lead to retinal iron accumulation and degeneration. High blood iron levels can occur in patients with hereditary hemochromatosis or result from use of iron supplements or multiple blood transfusions. Our results suggest that high blood iron levels may cause or exacerbate retinal disease.
Indexed as
Identifiers
What OpenQuestion holds
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.