Iron Chelation Therapy and Metabolic Control

Iron chelation therapy has emerged as a cornerstone in the management of disorders characterised by excess iron accumulation and associated metabolic dysregulation. Physiologically, iron is indispensable for oxygen transport, enzymatic reactions and mitochondrial respiration, yet its redox activity can catalyse the formation of reactive oxygen species, driving lipid peroxidation, protein oxidation and cellular injury. In clinical practice, chronic transfusion programmes for conditions such as thalassaemia major and myelodysplastic syndromes inevitably lead to tissue iron overload, with cardiac, hepatic and endocrine dysfunction. Chelating agents bind labile iron pools, facilitating urinary or faecal excretion and thereby restoring iron homeostasis. Beyond transfusional iron overload, dysregulated iron metabolism has been implicated in metabolic syndrome, diabetes and neurodegenerative diseases, prompting investigation of chelators for broader metabolic control. Advances in oral chelators have improved patient adherence and organ-specific clearance, while hybrid molecules that combine iron removal with antioxidant or anti-inflammatory properties are under development. Contemporary research explores the integration of chelation with modulation of the hepcidin-ferroportin axis to recalibrate systemic iron distribution and insulin sensitivity. These advances underscore the global importance of iron chelation not only in inherited and acquired iron loading conditions but also in the prevention of oxidative tissue damage in a range of metabolic disorders.

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Iron Chelation Therapy and Metabolic Control publication trend

The graph below shows the total number of articles in iron chelation therapy and metabolic control across all publications each year (not limited to Nature Index journals).

Technical terms

Iron overload: Accumulation of excess iron in tissues, leading to oxidative damage and organ dysfunction.

Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen that can damage lipids, proteins and DNA.

Ferroptosis: A form of regulated cell death driven by iron-dependent lipid peroxidation and loss of redox balance.

Hepcidin: A liver-derived peptide hormone that regulates systemic iron levels by controlling intestinal absorption and macrophage release.

Chelator: A compound that binds free metal ions, forming a stable complex to facilitate their removal from biological systems.

References

1. Iron Load Toxicity in Medicine: From Molecular and Cellular Aspects to Clinical Implications. International Journal of Molecular Sciences (2023).
2. The Vital Role Played by Deferiprone in the Transition of Thalassaemia from a Fatal to a Chronic Disease and Challenges in Its Repurposing for Use in Non-Iron-Loaded Diseases. Pharmaceuticals (2023).
3. Deferiprone–resveratrol hybrid attenuates iron accumulation, oxidative stress, and antioxidant defenses in iron-loaded human Huh7 hepatic cells. Frontiers in Molecular Biosciences (2024).
4. Iron Homeostasis in Health and Disease. International Journal of Molecular Sciences (2016).
5. Iron and Chelation in Biochemistry and Medicine: New Approaches to Controlling Iron Metabolism and Treating Related Diseases. Cells (2020).