Copper ion homeostasis

Copper ion homeostasis refers to the tightly regulated biological process that maintains appropriate intracellular and systemic concentrations of copper ions. This is essential because while copper is a vital trace element required for the function of numerous enzymes involved in redox reactions, mitochondrial respiration, melanin synthesis, collagen cross-linking, antioxidant defense (via superoxide dismutase), and iron metabolism (via ceruloplasmin), both deficiency and excess are harmful. The process involves coordinated uptake by transporters such as SLC31A1/CTR1; distribution via chaperones; storage mainly in the liver; incorporation into cuproenzymes; and excretion primarily through bile. Disruption leads to diseases such as Menkes disease (defective ATP7A transporter) or Wilson's disease (defective ATP7B transporter). Recent research has also linked dysregulated copper homeostasis with cancer progression—where targeting these pathways may offer therapeutic opportunities—and with neurodegenerative conditions. However, "Copper ion homeostasis" itself is not a single molecular target but rather a physiological process involving multiple proteins and pathways[1][2][3][4].

Other names

Copper homeostasisIntracellular copper ion homeostasisCellular copper balance

Supplementation to restore deficient copper-dependent enzyme activity (copper histidinate); Delivery of copper to cuproenzymes and induction of cuproptosis in cancer cells (elesclomol)