Iron Homeostasis and Ferroptosis in Human Diseases: Mechanisms and Therapeutic Prospects
Open accessAbstract
Iron, an essential mineral in the body, is involved in numerous physiological processes, making the maintenance of iron homeostasis crucial for overall health. Both iron overload and deficiency can cause various disorders and human diseases. Ferroptosis, a form of cell death dependent on iron, is characterized by the extensive peroxidation of lipids. Unlike other kinds of classical unprogrammed cell death, ferroptosis is primarily linked to disruptions in iron metabolism, lipid peroxidation, and antioxidant system imbalance. Ferroptosis is regulated through transcription, translation, and post-translational modifications, which affect cellular sensitivity to ferroptosis. Over the past decade or so, numerous diseases have been linked to ferroptosis as part of their etiology, including cancers, metabolic disorders, autoimmune diseases, central nervous system diseases, cardiovascular diseases, and musculoskeletal diseases. Ferroptosis-related proteins have become attractive targets for many major human diseases that are currently incurable, and some ferroptosis regulators have shown therapeutic effects in clinical trials although further validation of their clinical potential is needed. Therefore, in-depth analysis of ferroptosis and its potential molecular mechanisms in human diseases may offer additional strategies for clinical prevention and treatment. In this review, we discuss the physiological significance of iron homeostasis in the body, the potential contribution of ferroptosis to the etiology and development of human diseases, along with the evidence supporting targeting ferroptosis as a therapeutic approach. Importantly, we evaluate recent potential therapeutic targets and promising interventions, providing guidance for future targeted treatment therapies against human diseases.
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Ferroptosis is an iron-dependent RCD pathway characterized by lipid peroxidation and downregulation of antioxidant defense.
“Ferroptosis represents an iron-dependent RCD pathway characterized by lipid peroxidation and downregulation of the antioxidant defense of cells [39,40,41].”
From Role of Regulated Cell Death Pathways in Snakebite Envenomation: Mechanisms, Crosstalk, and Therapeutic Opportunities (2026) · cites this paper as [39]
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Iron metabolism in rheumatic diseases
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- Authors
- Ru, Q., Li, Y., Chen, L., Wu, Y., Min, J., & Wang, F.
- Affiliations
- Jianghan University (CN)
- Central South University (CN)
- First Affiliated Hospital Zhejiang University (CN)
- Zhejiang University (CN)
- Corresponding author
- Min, Junxia
- Wang, Fudi
- Venue
- Signal Transduction and Targeted Therapy
- Published
- 2024-10-14
- Volume
- 9
- Issue
- 1
- Pages
- 271-271
- ISSN
- 2059-3635 (ISSN-L)
- PMC
- PMC11486532
- OpenAlex
- W4403369705
- Cited by
- 724
- References
- 1,003
- Citations by year
- 2026: 407 · 2025: 310 · 2024: 7
- FWCI
- 53.50
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Signal Transduction and Targeted Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (32330047, 82072506, 82071970, 31970689)
- Natural Science Foundation of Hubei Province (2024AFB971)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Ferroptosis and cancer prognosis
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- iron homeostasis, ferroptosis, iron overload, iron deficiency, lipid peroxidation, antioxidant imbalance, ferroptosis regulators, cancer, metabolic disorders, autoimmune disease, central nervous system disorders, cardiovascular disease, musculoskeletal disorders, ferroptosis-targeted therapy
- MeSH terms
- Ferroptosis, Autoimmune Diseases, Cardiovascular Diseases, Homeostasis, Humans, Iron, Metabolic Diseases, Neoplasms, Lipid Peroxidation
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