Hyperferritinemia and inflammation
Open accessAbstract
Understanding of ferritin biology has traditionally centered on its role in iron storage and homeostasis, with low ferritin levels indicative of deficiency and high levels indicative of primary or secondary hemochromatosis. However, further work has shown that iron, redox biology and inflammation are inexorably linked. During infection, increased ferritin levels represent an important host defense mechanism that deprives bacterial growth of iron and protects immune cell function. It may also be protective, limiting the production of free radicals and mediating immunomodulation. Additionally, hyperferritinemia is a key acute-phase reactants, used by clinicians as an indication for therapeutic intervention, aimed at controlling inflammation in high-risk patients. One school of thought maintains that hyperferritinemia is an ‘innocent bystander’ biomarker of uncontrolled inflammation that can be used to gauge effectiveness of intervention. Other schools of thought maintain that ferritin induction could be a protective negative regulatory loop. Others maintain that ferritin is a key mediator of immune dysregulation, especially in extreme hyperferritinemia, via direct immune-suppressive and pro-inflammatory effects. There is a clear need for further investigation of the role of ferritin in uncontrolled inflammatory conditions both as a biomarker and mediator of disease because its occurrence identifies patients with high mortality risk and its resolution predicts their improved survival.
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Ferritin heavy chain-mediated iron delivery and storage are critical for oligodendrocyte iron metabolism and myelin lipid synthesis, helping to constrain iron-driven lipid peroxidation and ferroptotic death in white matter.
“ferritin heavy chain–mediated iron delivery and storage are critical for oligodendrocyte iron metabolism and myelin lipid synthesis, helping to constrain iron-driven lipid peroxidation and ferroptotic death in white matter [88, 89]”
From PLCγ2 deficiency compromises systemic immune tolerance and erodes myelin homeostasis while enhancing oxidative metabolism in the mouse brain (2026) · cites this paper as [88]
The “Ferritin in iron homeostasis” section says heavy-chain ferritin is required for iron loading and helps quench oxidative stress. The paper also describes ferritin limiting lipid peroxidation in a macrophage-related context. It does not establish the claimed role in oligodendrocyte iron metabolism, myelin lipid synthesis, or prevention of ferroptotic death in white matter. (LLM, conf=0.87)
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References 111 · Cited by 638
- Authors
- Kernan, K. F., & Carcillo, J. A.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Carcillo, Joseph A
- Venue
- International Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2017-05-25
- Volume
- 29
- Issue
- 9
- Pages
- 401-409
- ISSN
- 0953-8178 (ISSN-L)
- 1460-2377
- PMC
- PMC5890889
- OpenAlex
- W2617626520
- Cited by
- 638
- References
- 111
- Citations by year
- 2026: 52 · 2025: 69 · 2024: 89 · 2023: 117 · 2022: 131 · 2021: 85 · 2020: 68 · 2019: 21 · 2018: 6
- FWCI
- 4.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Immunology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM108168)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Ferroptosis and cancer prognosis
- Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
- Keywords
- hyperferritinemia, ferritin, inflammation, iron homeostasis, acute phase proteins, infection, host defense, redox biology, immunomodulation, biomarkers, immune dysregulation, iron sequestration, hemochromatosis
- MeSH terms
- Acute-Phase Reaction, Animals, Cataract, Ferritins, Hemochromatosis, Humans, Immunity, Innate, Inflammation, Iron, Iron Metabolism Disorders, Immunomodulation
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