NCOA4 deficiency impairs systemic iron homeostasis
Open accessAbstract
The cargo receptor NCOA4 mediates autophagic ferritin degradation. Here we show that NCOA4 deficiency in a knockout mouse model causes iron accumulation in the liver and spleen, increased levels of transferrin saturation, serum ferritin, and liver hepcidin, and decreased levels of duodenal ferroportin. Despite signs of iron overload, NCOA4-null mice had mild microcytic hypochromic anemia. Under an iron-deprived diet (2-3 mg/kg), mice failed to release iron from ferritin storage and developed severe microcytic hypochromic anemia and ineffective erythropoiesis associated with increased erythropoietin levels. When fed an iron-enriched diet (2 g/kg), mice died prematurely and showed signs of liver damage. Ferritin accumulated in primary embryonic fibroblasts from NCOA4-null mice consequent to impaired autophagic targeting. Adoptive expression of the NCOA4 COOH terminus (aa 239-614) restored this function. In conclusion, NCOA4 prevents iron accumulation and ensures efficient erythropoiesis, playing a central role in balancing iron levels in vivo.
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In iron-loaded cells, turnover of NCOA4 is greatly enhanced to block ferritin degradation and increase iron storage.
“Conversely, in iron-loaded cells the turnover of NCOA4 is greatly enhanced to block ferritin degradation and thus increase iron storage (Mancias et al., 2014, 2015; Bellelli et al., 2016; Santana-Codina and Mancias, 2018).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Bellelli et al., 2016
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- Authors
- Bellelli, R., Federico, G., Matte’, A., Colecchia, D., Iolascon, A., Chiariello, M., Santoro, M., De Franceschi, L., & Carlomagno, F.
- Affiliations
- Institute for Experimental Endocrinology and Oncology (IT)
- Istituto di Fisiologia Clinica (IT)
- Corresponding author
- Carlomagno, Francesca
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2016-01
- Volume
- 14
- Issue
- 3
- Pages
- 411-421
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2234023838
- Cited by
- 248
- References
- 31
- Citations by year
- 2026: 22 · 2025: 26 · 2024: 38 · 2023: 29 · 2022: 32 · 2021: 23 · 2020: 24 · 2019: 18 · 2018: 13 · 2017: 19 · 2016: 4
- FWCI
- 17.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- INFM-OAR (INFN Catania) (submittedVersion, cc-by-nc-nd)
- Funders
- Regione Campania
- Associazione Italiana per la Ricerca sul Cancro
- Ministero dell'Università e della Ricerca
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- NCOA4, iron homeostasis, ferritin degradation, autophagy, iron overload, hepcidin, ferroportin, microcytic hypochromic anemia, ineffective erythropoiesis, erythropoietin, liver injury, iron deficiency, iron accumulation
- MeSH terms
- Anemia, Hypochromic, Animals, Autophagy, Cell Line, Duodenum, Erythrocytes, Erythropoiesis, Female, Ferritins, Iron, Liver, Male, Oxidoreductases, Spleen, Up-Regulation, Reactive Oxygen Species, Mice, Knockout, Iron Overload, Iron, Dietary, Mice, Nuclear Receptor Coactivators, Hepcidins
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