Disruption of ceruloplasmin and hephaestin in mice causes retinal iron overload and retinal degeneration with features of age-related macular degeneration
Open accessAbstract
Mechanisms of brain and retinal iron homeostasis have become subjects of increased interest after the discovery of elevated iron levels in brains of patients with Alzheimer's disease and retinas of patients with age-related macular degeneration. To determine whether the ferroxidase ceruloplasmin (Cp) and its homolog hephaestin (Heph) are important for retinal iron homeostasis, we studied retinas from mice deficient in Cp and/or Heph . In normal mice, Cp and Heph localize to Müller glia and retinal pigment epithelium, a blood–brain barrier. Mice deficient in both Cp and Heph , but not each individually, had a striking, age-dependent increase in retinal pigment epithelium and retinal iron. The iron storage protein ferritin was also increased in Cp –/– Heph –/ Y retinas. After retinal iron levels had increased, Cp –/– Heph –/ Y mice had age-dependent retinal pigment epithelium hypertrophy, hyperplasia and death, photoreceptor degeneration, and subretinal neovascularization, providing a model of some features of the human retinal diseases aceruloplasminemia and age-related macular degeneration. This pathology indicates that Cp and Heph are critical for CNS iron homeostasis and that loss of Cp and Heph in the mouse leads to age-dependent retinal neurodegeneration, providing a model that can be used to test the therapeutic efficacy of iron chelators and antiangiogenic agents.
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Retinal iron levels increase with age, iron is significantly implicated in AMD, and iron chelation may help to reverse the process.
“Retinal iron levels increase with age [1322], iron is significantly implicated in AMD [1323-1329], and iron chelation may help to reverse the process [1330].”
From Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases (2009) · cites this paper as [1326]
Gene-ablation murine models and patients deficient in CP and HEPH present with iron-deficient anemia, demonstrating the importance of these oxidases for iron export.
“The importance of these oxidases for successful iron export into the circulation has been demonstrated with gene-ablation murine models as well as identification of patients deficient in CP and HEPH, presenting with iron-deficient anemia (Yoshida et al., 1995; Hahn et al., 2004).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Hahn et al., 2004
By 5-6 months of age, the Cp−/−Heph−/Y mice had increased iron levels, and the highest iron levels were in the RPE and photoreceptor OS.
“By 5–6 months of age, the Cp−/−Heph−/Y mice had increased iron levels, and the highest iron levels were in the RPE and photoreceptor OS.”
From Retinal ultrastructure of murine models of dry age-related macular degeneration (AMD) (2010) · cites this paper as Hahn et al., 2004
At 6-9 months old, Cp−/−Heph−/Y mice had severe retinal degeneration with RPE hypopigmentation, hypertrophy, hyperplasia, and necrosis.
“At 6–9 months old, Cp−/−Heph−/Y mice had severe retinal degeneration with RPE hypopigmentation, hypertrophy, hyperplasia, and necrosis.”
From Retinal ultrastructure of murine models of dry age-related macular degeneration (AMD) (2010) · cites this paper as Hahn et al., 2004
Evidence of focal CNV was present in 75% of 12-13 month-old Cp−/−Heph−/Y mice and 50% of 7-9 month-old mice.
“Evidence of focal CNV was also present in 75% of 12–13 month-old mice and 50% of 7–9 month-old mice (Hahn et al., 2004; Hadziahmetovic et al., 2008).”
From Retinal ultrastructure of murine models of dry age-related macular degeneration (AMD) (2010) · cites this paper as Hahn et al., 2004
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- Authors
- Hahn, P., Qian, Y., Dentchev, T., Chen, L., Beard, J., Harris, Z. L., & Dunaief, J. L.
- Affiliations
- Pennsylvania State University (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2004-09-13
- Volume
- 101
- Issue
- 38
- Pages
- 13850-13855
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC518844
- OpenAlex
- W1494802998
- Cited by
- 264
- References
- 30
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 5 · 2023: 7 · 2022: 8 · 2021: 14 · 2020: 14 · 2019: 9 · 2018: 12 · 2017: 10 · 2016: 10 · 2015: 16 · 2014: 16 · 2013: 11 · 2012: 18
- FWCI
- 8.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Investigative Ophthalmology & Visual Science
- Funders
- F. M. Kirby Foundation
- Research to Prevent Blindness
- Retina Research Foundation
- James N. Kirby Foundation
- National Institutes of Health (5k08dk002464-04, DK02464)
- National Eye Institute (EY 015240, EY00417, K08EY000417, R01EY015240)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK058086, DK02464)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Keywords
- ceruloplasmin, hephaestin, ferroxidase, age-related macular degeneration, aceruloplasminemia, retinal pigment epithelium, photoreceptor degeneration, subretinal neovascularization, ferritin, Müller cells, retinal degeneration, iron chelators, anti-angiogenic therapy, mouse model
- MeSH terms
- Animals, Ceruloplasmin, Crosses, Genetic, Macular Degeneration, Membrane Proteins, Mice, Inbred C57BL, Retinal Degeneration, Vitamin A, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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