The DOI matches its Crossref record; 127 of the 127 references it cites were found in a registry or an index.
Impaired Iron Status in Aging Research
Open accessAbstract
Aging is associated with disturbances in iron metabolism and storage. During the last decade, remarkable progress has been made toward understanding their cellular and molecular mechanisms in aging and age-associated diseases using both cultured cells and animal models. The field has moved beyond descriptive studies to potential intervention studies focusing on iron chelation and removal. However, some findings remain controversial and inconsistent. This review summarizes important features of iron dyshomeostasis in aging research with a particular emphasis on current knowledge of the mechanisms underlying age-associated disorders in rodent models.
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![Figure 1 Cellular labile iron pool. The transferrin-transferrin receptor (Tf-TfR) pathway is the primary route of cellular iron acquisition [67]. Cells assimilate iron when Fe3+-Tf binds to TfR at the cell surface, and the complex is internalized into endosomes. Endosomal acidification promotes iron to dissociate from Tf, and the metal is then reduced to Fe2+ and transported into the cytosol by the transmembrane protein divalent metal transporter 1 (DMT1) and Zip14. The non-Tf-bound iron pathway, the shaded area, appears mainly during states of iron overload. Much of the iron normally assimilated by cells is destined to the mitochondria via mitoferrin, the site of heme and iron-sulfur cluster biosynthesis. Iron is exported from the mitochondria in the form of iron-sulfur clusters or heme. Export of iron-sulfur clusters involves ABCB7. Cells export iron through ferroportin. The absence of ferroportin in skeletal muscles and other post-mitotic tissues may result in iron accumulation over time.](/paper-figures/60176acef83e453dbade0247bc71de97/impaired-iron-status-in-aging-research-figure-1.jpg)
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“Age-dependent accumulation of iron in various tissues has been reported to occur separately to the enrichment of senescent cells [11], [12], [16], [17], [18], [19].”
From Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis (2018) · cites this paper as [12]
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“Conceivably, senescent cells account for the increased iron observed in aged tissues [11], [12] and similarly in organs affected by age-related pathologies [13], [14], [15].”
From Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis (2018) · cites this paper as [12]
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Research works printed but not linked: 1
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The role of iron in brain ageing and neurodegenerative disorders
Ward, R. J., Zucca, F. A., Duyn, J. H., Crichton, R. R., & Zecca, L. (2014) · The Lancet Neurology · doi:10.1016/s1474-4422(14)70117-6 · Cited by 1,819
Interactions of iron, dopamine and neuromelanin pathways in brain aging and Parkinson's disease
Zucca, F. A., Segura-Aguilar, J., Ferrari, E., Muñoz, P., Paris, I., Sulzer, D., Sarna, T., Casella, L., & Zecca, L. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2015.09.012 · Cited by 659
Metal Toxicity Links to Alzheimer's Disease and Neuroinflammation
Huat, T. J., Camats‐Perna, J., Newcombe, E. A., Valmas, N., Kitazawa, M., & Medeiros, R. (2019) · Journal of Molecular Biology · doi:10.1016/j.jmb.2019.01.018 · Cited by 501
Ferroptosis and Its Role in Diverse Brain Diseases
Weiland, A., Wang, Y., Wu, W., Lan, X., Han, X., Li, Q., & Wang, J. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1403-3 · Cited by 473
Masaldan, S., Clatworthy, S. A. S., Gamell, C., Meggyesy, P. M., Rigopoulos, A.-T., Haupt, S., Haupt, Y., Denoyer, D., Adlard, P. A., Bush, A. I., et al. (2018) · Redox Biology · doi:10.1016/j.redox.2017.08.015 · Cited by 452
Metadata
- Authors
- Xu, J., Jia, Z., Knutson, M. D., & Leeuwenburgh, C.
- Affiliations
- University of Florida (US)
- Corresponding author
- Xu, Jinze
- Leeuwenburgh, Christiaan
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2012-02-22
- Volume
- 13
- Issue
- 2
- Pages
- 2368-2386
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC3292028
- OpenAlex
- W2144968983
- Cited by
- 103
- References
- 127
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 10 · 2023: 14 · 2022: 8 · 2021: 12 · 2020: 8 · 2019: 6 · 2018: 10 · 2017: 5 · 2016: 2 · 2015: 5 · 2014: 5 · 2013: 7 · 2012: 2
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- American Heart Association
- University of Florida (P30 AG028740)
- National Institutes of Health (UL1TR000064, DK080706)
- National Institute on Aging (R01AG017994, P30AG028740)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK080706)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- iron metabolism, iron dyshomeostasis, aging, age-related diseases, iron chelation, iron storage, rodent models, cellular and molecular mechanisms
- MeSH terms
- Aging, Animals, Disease Models, Animal, Health Status, Humans, Iron, Mitochondria, Rodentia, Iron Metabolism Disorders
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