Systemic iron pool and iron-dependent proteins

The systemic iron pool and iron-dependent proteins represent the collective components of iron metabolism and utilization in the human body. Iron is an essential micronutrient required for critical biological processes, including oxygen transport via hemoglobin and myoglobin, electron transfer in the mitochondrial respiratory chain via cytochromes, and DNA synthesis via ribonucleotide reductase (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9650165/; Ovid, https://journals.lww.com/ccmjournal/Abstract/2019/03000/Iron_and_the_Pulmonary_Vasculature.15.aspx). The systemic iron pool, which includes iron bound to transferrin in circulation and stored within ferritin in tissues, is tightly regulated by the hepcidin-ferroportin axis (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5503768/). Hepcidin, the master regulator, controls iron flux by inducing the degradation of the iron exporter ferroportin on enterocytes and macrophages (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461214/). Dysregulation of this system leads to significant pathologies, such as iron deficiency anemia or iron overload disorders like hereditary hemochromatosis and transfusion-dependent thalassemias (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9650165/). Therapeutic interventions include iron supplements to replenish the pool, iron chelators to remove toxic excess iron, and emerging agents like hepcidin mimetics to modulate iron distribution (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461214/; MDPI, https://www.mdpi.com/1422-0067/23/19/11153). This target group is central to maintaining metabolic health and preventing the toxic effects of free iron-mediated oxidative stress (Frontiers, https://www.frontiersin.org/articles/10.3389/fcell.2022.990327/full).

Other names

Iron metabolismIron homeostasisLabile iron poolIron-containing proteinsSystemic iron regulation

Modulation of systemic iron levels through chelation of excess iron, supplementation of deficient iron stores, or regulation of the hepcidin-ferroportin axis to control iron flux.