Deciphering the role of hepcidin in iron metabolism and anemia management

One of the most common diseases worldwide is anemia, which is characterized by insufficient erythrocyte production. Numerous complex factors, such as chronic diseases, genetic mutations, and nutritional inadequacies, contribute to this widespread syndrome. This review focuses specifically on anemias caused by defective hepcidin production. Hepcidin, a peptide hormone produced primarily by liver cells, plays a crucial role in regulating iron levels by controlling its absorption. Hepcidin's mechanism of action involves binding to the ferroportin iron transporter, causing its internalization. Disturbances in iron metabolism can have far-reaching consequences, affecting not only the blood but also organs like the liver, kidneys, and brain. Iron homeostasis is crucial for maintaining optimal physiological function. Several blood-based markers are employed to assess iron stores. However, these markers have inherent limitations. Hepcidin, a key regulator of iron metabolism, plays a pivotal role in preventing iron release into the plasma from absorptive enterocytes and macrophages. Elucidating the structure and function of hepcidin is essential for understanding its role in iron homeostasis, which has significant implications for the diagnosis and management of various anemia subtypes. A well-established correlation exists between hepcidin dysregulation and iron deficiency. Despite its potential as a biomarker, the clinical application of hepcidin is hindered by the lack of a commercially available, clinically validated assay. This review aims to provide a comprehensive overview of hepcidin's role in regulating blood iron concentrations and elucidate its implications in the pathogenesis of various anemia subtypes, paving the way for its future applications in research and clinical practice.