Copper metabolism pathway

The "Copper metabolism pathway" refers to the highly regulated cellular and systemic processes responsible for copper uptake, distribution, utilization, storage, and excretion. Key proteins include transporters like copper transporter 1 (CTR1), ATPases (ATP7A, ATP7B), chaperones (ATOX1, CCS, COX17), and enzymes (cuproenzymes such as cytochrome c oxidase, lysyl oxidase, superoxide dismutase, ceruloplasmin, and multicopper oxidases). Copper metabolism supports essential functions including electron transport in mitochondria, antioxidative defense, connective tissue integrity, and iron metabolism. Dysregulation is associated with rare genetic diseases (Menkes, Wilson) as well as common pathologies such as cancer, neurodegeneration, and cardiovascular disease. While components of copper metabolism (e.g., CTR1, ATP7B, specific cuproenzymes) can be considered drug targets, the pathway as a whole is too broad to represent a single targetable entity.

Other names

Copper homeostasis pathwayCopper metabolic pathwayCopper homeostasisCopper trafficking pathwayCopper metabolism

Chelation of copper to reduce copper availability for essential metalloenzymes, leading to impaired growth in malignancies dependent on copper. Ionophore-mediated copper transport into cells to increase cytotoxic free copper and induce oxidative damage and cuproptosis (copper-dependent cell death). Alteration of angiogenesis via copper-dependent mechanisms. Modulation of redox status through superoxide dismutase inhibition/activation.