Iron Homeostasis and the Inflammatory Response
Open accessAbstract
Iron and its homeostasis are intimately tied to the inflammatory response. The adaptation to iron deficiency, which confers resistance to infection and improves the inflammatory condition, underlies what is probably the most obvious link: the anemia of inflammation or chronic disease. A large number of stimulatory inputs must be integrated to tightly control iron homeostasis during the inflammatory response. In order to understand the pathways of iron trafficking and how they are regulated, this article presents a brief overview of iron homeostasis. A major focus is on the regulation of the peptide hormone hepcidin during the inflammatory response and how its function contributes to the process of iron withdrawal. The review also summarizes new and emerging information about other iron metabolic regulators and effectors that contribute to the inflammatory response. Potential benefits of treatment to ameliorate the hypoferremic condition promoted by inflammation are also considered.
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Free iron can catalyze formation of reactive oxygen species and must be safely bound by specialized proteins.
“Also free iron can catalyze formation of reactive oxygen species (ROS) and must be safely bound by specialized proteins.”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Wessling-Resnick, 2010
Compared to other metals, the body contains much higher levels of iron (3.5-4 g versus 100 mg copper), aqueous ferric ions have low solubility, and excess iron is not actively excreted via the kidney.
“However, compared to other metals, the body contains much higher levels of iron (3.5 -4 g of iron versus 100 mg of copper), aqueous ferric ions exhibit low solubility and unlike other metals, excess iron is not actively excreted via the kidney.”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Wessling-Resnick, 2010
Section II, “Iron homeostasis: a brief overview” (page unavailable), describes iron recycling and regulation through intestinal absorption, but does not give the claimed iron and copper quantities or address aqueous ferric-ion solubility or active renal excretion. Searches for the quantities, copper, solubility, and excretion found no passage establishing those claims. (LLM, conf=0.76)
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- Authors
- Wessling-Resnick, M.
- Affiliations
- Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115;
- Venue
- Annual Review of Nutrition
- Publisher
- Annual Reviews
- Published
- 2010-07-01
- Volume
- 30
- Issue
- 1
- Pages
- 105-122
- ISSN
- 0199-9885 (ISSN-L)
- 1545-4312
- PMC
- PMC3108097
- OpenAlex
- W2141337211
- Cited by
- 480
- References
- 43
- Citations by year
- 2026: 21 · 2025: 34 · 2024: 37 · 2023: 26 · 2022: 51 · 2021: 32 · 2020: 45 · 2019: 34 · 2018: 34 · 2017: 27 · 2016: 15 · 2015: 22 · 2014: 30 · 2013: 18 · 2012: 23
- FWCI
- 3.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (R21DA025573, R03DA027030)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK064750, RC1DK086774)
- National Institute of Environmental Health Sciences (R01ES014638)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Ferroptosis and cancer prognosis
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- iron homeostasis, inflammation, hepcidin, anemia of chronic disease, chronic disease, iron deficiency, iron trafficking, hypoferremia, infection resistance
- MeSH terms
- Iron Deficiencies, Chronic Disease, Homeostasis, Humans, Inflammation, Iron, Anemia, Iron-Deficiency, Antimicrobial Cationic Peptides, Hepcidins
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