Journal
ANNUAL REVIEW OF NUTRITION, VOL 30
Volume 30, Issue -, Pages 105-122Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.nutr.012809.104804
Keywords
hepcidin; anemia of chronic disease; iron withdrawal; iron overload; hemochromatosis; infection
Categories
Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK064750, RC1DK086774] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES014638] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R21DA025573, R03DA027030] Funding Source: NIH RePORTER
- NIDA NIH HHS [R21 DA025573, R21 DA025573-02, R03 DA027030-02, R03 DA027030] Funding Source: Medline
- NIDDK NIH HHS [RC1 DK086774-02, R01 DK064750, RC1 DK086774, R01 DK064750-06] Funding Source: Medline
- NIEHS NIH HHS [R01 ES014638-07, R01 ES014638] Funding Source: Medline
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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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