Abstract
Iron is a critical metal for several vital biological processes. Most of the body’s iron is bound to hemoglobin in erythrocytes. Iron from senescent red blood cells is recycled by macrophages in the spleen, liver and bone marrow. Dietary iron is taken up by the divalent metal transporter 1 (DMT1) in enterocytes and transported to portal blood via ferroportin (FPN), where it is bound to transferrin and taken up by hepatocytes, macrophages and bone marrow cells via transferrin receptor 1 (TfR1). While most of the physiologically active iron is bound hemoglobin, the major storage of most iron occurs in the liver in a ferritin-bound fashion. In response to an increased iron load, hepatocytes secrete the peptide hormone hepcidin, which binds to and induces internalization and degradation of the iron transporter FPN, thus controlling the amount of iron released from the cells into the blood. This review summarizes the key mechanisms and players involved in cellular and systemic iron regulation.
Highlights
Iron (Fe) is one of the most abundant elements of the Earth’s crust [1]
Most of this iron is required for erythropoiesis, which is the production of oxygen-transporting red blood cells [13,14]
Erythrocyte precursors in the bone marrow are restricted to take up transferrin-bound iron via transferrin receptor 1 (TfR1), as they express high levels of TfR1, whereas hepatocytes and other non-erythroid cells are able to use non-transferrin bound iron (NTBI) and other sources of iron as they express other transporters [23]
Summary
Iron (Fe) is one of the most abundant elements of the Earth’s crust [1]. As a transition metal, its ability to donate and accept electrons in redox reactions, makes it favorable for fundamental biological processes [2]. Iron is one of the most important metals to sustain life from single cell bacteria to multi-cellular organisms such as humans [3,4] This metal plays a vital role in several cellular processes such as DNA synthesis, nucleic acid repair, cellular respiration in mitochondria, cell growth and cell death and contributes to host defense and cell signaling [1,2]. The hydroxyl radical is known as one of the most dominant oxidants found in the human body attacking proteins, lipids, nucleic acids and carbohydrates leading to peroxidation and cell apoptosis [3]. Persistent iron deficiency even without anemia has been associated with fatigue, poorer cognitive and motor skills, defective immune cell function and increased disease severity in heart failure [11]
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