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Systemic iron deficiency is a pathological state characterized by insufficient iron to meet the body's physiological requirements, progressing from depleted stores to iron deficiency anemia [1, 6]. It is not a specific molecular target but a clinical condition resulting from an imbalance in iron homeostasis, often caused by inadequate intake, malabsorption, or chronic blood loss [2, 4]. Iron is an essential element for life, serving as a central component of hemoglobin for oxygen transport and as a cofactor for enzymes involved in DNA synthesis and mitochondrial energy production [3, 5]. Therapeutic strategies focus on iron replacement via oral or intravenous routes to restore systemic levels [4]. In many chronic diseases, iron deficiency is driven by the hormone hepcidin, which inhibits iron entry into the plasma, making the hepcidin-ferroportin axis a key area for pharmacological intervention [5, 6].
Pharmacological management involves the administration of exogenous iron to replenish systemic stores for incorporation into hemoglobin and other iron-dependent proteins, or the modulation of regulatory pathways such as the hepcidin-ferroportin axis to improve iron bioavailability [4, 5, 6].
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