Cuproptosis

Cuproptosis is a form of controlled cell death driven by copper. It is distinct from other death programs like apoptosis, ferroptosis, necroptosis, and pyroptosis. Here is how it works. Copper inside one of your cells is normally held by handler proteins (chaperones like ATOX1 and CCS). When it rises beyond what they can buffer, the loose copper binds certain proteins in the mitochondria's TCA cycle. The main target is a lipoylated enzyme called DLAT (dihydrolipoamide S-acetyltransferase). The copper makes DLAT clump. That clumping also brings a loss of iron-sulfur cluster proteins. The result is protein-toxicity stress, mitochondrial failure, and cell death. A mitochondrial enzyme called FDX1 is needed for the lipoylation. So FDX1 acts as a key upstream switch. Cells with active oxidative phosphorylation and lots of lipoylated proteins are especially vulnerable. Cuproptosis has drawn interest as a possible weak spot in copper-handling cancers. And it is relevant to metabolic and brain conditions too.

Last reviewed: June 22, 2026

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