Fig. 3: Copper dyshomeostasis promotes atherosclerosis through oxidative stress. | Cell Death Discovery

Fig. 3: Copper dyshomeostasis promotes atherosclerosis through oxidative stress.

From: Copper homeostasis and cuproptosis in atherosclerosis: metabolism, mechanisms and potential therapeutic strategies

Fig. 3

Excessive copper interacts with H2O2 via the Fenton reaction, generating highly reactive hydroxyl radicals. These radicals induce lipid peroxidation, DNA strand breaks, and base oxidation and impair the function of antioxidant enzymes, ultimately leading to increased oxidative stress and potential damage to cells. On the other hand, copper deficiency also impairs the function of certain antioxidant enzymes, causing a decrease in SOD1 and COX activity. This reduced activity results in lowered NO levels, inactivation of complex I, and increased production of ROS, thereby exacerbating oxidative stress within cells. Together, these processes promote the development of atherosclerosis. Figure created with BioRender. SLC31A1 solute carrier family 31 member 1, STEAP six-transmembrane epithelial antigen of the prostate, H2O2 hydrogen peroxide, •OH reactive hydroxyl radicals, ROS reactive oxygen species, ATP7A and ATP7B ATPase copper transporter 7A and 7B, CAT catalase, GSH-Px glutathione peroxidase, CP ceruloplasmin, LOX lysyl oxidase, SOD1 superoxide dismutase 1, COX cytochrome c oxidase, and AS atherosclerosis.

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