Iron is an important micronutrient required in various physiological functions, including oxygen transport, energy metabolism, immune function, and DNA synthesis. It can alternate between ferrous and ferric states which enables it to participate in redox reactions necessary for cellular homeostasis. The human body maintains delicate of iron through regulated absorption, transport, storage, and recycling mechanisms. Important proteins like hepcidin, ferroportin, transferrin, and ferritin coordinate for iron regulation. Hepcidin acts as a master regulator by inhibiting iron export during sufficient iron status or inflammation. Imbalance in iron homeostasis can lead to clinical conditions such as iron deficiency anemia (IDA) and anemia of chronic disease (ACD). IDA is generally caused by inadequate dietary intake, impaired absorption, or chronic blood loss, while ACD results from inflammatory-mediated iron sequestration despite adequate stores. Accurate diagnosis depends on a combination of biomarkers such as serum ferritin, transferrin saturation, soluble transferrin receptor (sTfR), and hepcidin levels. Treatment strategies include dietary modifications and oral iron supplements to intravenous iron and erythropoiesis-stimulating agents. Emerging therapies targeting hepcidin and iron-regulatory pathways offer promising alternatives for refractory cases. Furthermore, iron overload disorders such as hereditary hemochromatosis and transfusional hemosiderosis require careful monitoring and management to prevent oxidative damage. Advances in molecular biology and iron-targeted therapeutics are paving the way for personalized treatment approaches. This chapter provides an in-depth overview of iron metabolism, its critical roles in health and disease, and the evolving landscape of diagnosis and treatment of anemia and iron-related disorders.

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Iron Metabolism and Its Role in Anemia

  • Jyoti Upadhyay,
  • Tarnjot Kaur,
  • Mukesh Nandave

摘要

Iron is an important micronutrient required in various physiological functions, including oxygen transport, energy metabolism, immune function, and DNA synthesis. It can alternate between ferrous and ferric states which enables it to participate in redox reactions necessary for cellular homeostasis. The human body maintains delicate of iron through regulated absorption, transport, storage, and recycling mechanisms. Important proteins like hepcidin, ferroportin, transferrin, and ferritin coordinate for iron regulation. Hepcidin acts as a master regulator by inhibiting iron export during sufficient iron status or inflammation. Imbalance in iron homeostasis can lead to clinical conditions such as iron deficiency anemia (IDA) and anemia of chronic disease (ACD). IDA is generally caused by inadequate dietary intake, impaired absorption, or chronic blood loss, while ACD results from inflammatory-mediated iron sequestration despite adequate stores. Accurate diagnosis depends on a combination of biomarkers such as serum ferritin, transferrin saturation, soluble transferrin receptor (sTfR), and hepcidin levels. Treatment strategies include dietary modifications and oral iron supplements to intravenous iron and erythropoiesis-stimulating agents. Emerging therapies targeting hepcidin and iron-regulatory pathways offer promising alternatives for refractory cases. Furthermore, iron overload disorders such as hereditary hemochromatosis and transfusional hemosiderosis require careful monitoring and management to prevent oxidative damage. Advances in molecular biology and iron-targeted therapeutics are paving the way for personalized treatment approaches. This chapter provides an in-depth overview of iron metabolism, its critical roles in health and disease, and the evolving landscape of diagnosis and treatment of anemia and iron-related disorders.