Fig. 1: Intake, absorption, excretion of copper ions, and their regulation of bone metabolism. | Cell Death Discovery

Fig. 1: Intake, absorption, excretion of copper ions, and their regulation of bone metabolism.

From: Emerging regulated cell death mechanisms in bone remodeling: decoding ferroptosis, cuproptosis, disulfidptosis, and PANoptosis as therapeutic targets for skeletal disorders

Fig. 1

The dietary Cu2+ is first converted to Cu+ by metalloreductases from the STEAP family. Following, the Cu+ is taken up by epithelial cells in the small intestine via the SLC31A1, also referred to as CTR1. ATP7A delivers copper to the bloodstream and guides it to the trans-Golgi network and vesicles.ATP7B manages the export of intracellular copper. In the cytoplasm, the copper chaperone for CCS guides copper ions to SOD1. SOD1 converts O2- into oxygen O2 and H2O2. FDX1 serves as a reductase converting Cu2+ to the more toxic Cu+, and acts as an essential upstream regulator of lipoic acid synthesis and protein lipoylation. COX17 facilitates copper into mitochondria. Inside the mitochondria, copper contributes to the synthesis of SCO1 and SCO2, aiding in the assembly of MT-CO2, also referred to as COX2.

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