Iron Metabolism and Oxidative Stress in Health and Disease

Iron is indispensable for oxygen transport, DNA synthesis and mitochondrial respiration. Yet excess or mis-distributed iron catalyses the formation of reactive oxygen species (ROS), driving lipid peroxidation, protein oxidation and DNA damage. A tightly regulated axis of intestinal absorption, systemic circulation, cellular uptake and storage governs iron homeostasis through key players such as hepcidin, ferroportin and ferritin. Disruption of this axis underlies a spectrum of conditions—from iron deficiency anaemia and neurodegenerative disorders to hereditary haemochromatosis and cardiomyopathy—where oxidative stress exacerbates tissue injury and dysfunction. Conversely, strategic modulation of iron availability and antioxidant defences offers therapeutic promise. Recent progress has illuminated molecular mechanisms linking iron-driven redox imbalance to inflammation, cell death modalities such as ferroptosis and ageing-associated pathologies, emphasising the need for integrative approaches that span nutritional, genetic and pharmacological interventions.

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Iron Metabolism and Oxidative Stress in Health and Disease publication trend

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Technical terms

Reactive oxygen species (ROS): Chemically reactive molecules derived from oxygen, including superoxide and hydrogen peroxide, that can damage biomolecules.

Hepcidin: A liver-derived peptide hormone that regulates systemic iron export by inducing degradation of the iron transporter ferroportin.

Labile iron pool: The readily exchangeable and redox-active fraction of intracellular iron that participates in metabolic processes and can catalyse ROS formation.

Ferroptosis: An iron-dependent form of regulated cell death characterised by lipid peroxidation and loss of redox homeostasis.

References

1. Oxidative Status, Iron Plasma Levels in Venous Thrombosis Patients. Antioxidants (2024).
2. A genetically encoded probe for monitoring and detection of iron in real-time. Sensors & Diagnostics (2024).
3. Aberrant Transferrin and Ferritin Upregulation Elicits Iron Accumulation and Oxidative Inflammaging Causing Ferroptosis and Undermines Estradiol Biosynthesis in Aging Rat Ovaries by Upregulating NF-Κb-Activated Inducible Nitric Oxide Synthase: First Demonstration of an Intricate Mechanism. International Journal of Molecular Sciences (2022).