Copper metabolism regulation

Copper metabolism regulation as a concept encompasses the pathways, proteins, and molecular mechanisms that maintain copper homeostasis in mammals. Absorption occurs in the small intestine via copper transporters including CTR1 (SLC31A1), CTR2, and DMT1, often aided by reduction of Cu²⁺ to Cu⁺ by metalloreductases such as STEAP and DCYTB[2][3][4][5]. In the circulation, copper is bound to albumin and ceruloplasmin, and distributed to tissues such as the liver, which serves as the main storage and regulatory organ[1][3][5]. Intracellular chaperones such as COX17, ATOX1, and CCS deliver copper to enzymes (e.g., cytochrome c oxidase, superoxide dismutase, lysyl oxidase), which are essential for cellular energy production, antioxidative defense, and connective tissue structure[3][5][6][7]. Efflux from cells and excretion via bile are mediated by ATP7A and ATP7B. Dysregulation leads to human diseases such as Wilson’s disease (copper overload, often in liver/brain), Menkes disease (copper deficiency), neurologic disorders, and cancer[1][2][3][7]. As "copper metabolism regulation" refers collectively to these pathways and not a standard molecular drug target, this entry is not specific enough to directly map to a canonical target or abbreviation and should be reconciled to the relevant specific proteins or enzymes in structured data.

Other names

Copper homeostasisCopper regulationCopper metabolic pathway

Chelation and removal of copper; Promoting copper excretion via bile; Inhibition of copper absorption; Copper ionophore-mediated delivery to trigger cell death (cuproptosis)