Fig. 2: Oxidative stress induced by copper-induced cell death in CVD. | Cell Death & Disease

Fig. 2: Oxidative stress induced by copper-induced cell death in CVD.

From: Copper homeostasis and copper-induced cell death in the pathogenesis of cardiovascular disease and therapeutic strategies

Fig. 2

Excess copper results in the oxidation of catecholamines by promoting GSH oxidation. Through the Fenton reaction, copper produces oxidative stress, increasing lipid metabolism dysfunction and leading to DNA breakage. Copper ions directly bind fatty acylation components in the TCA cycle, leading to the aggregation and dysregulation of these proteins, blocking the TCA cycle of the tricarboxylic acid cycle, triggering proteotoxic stress, and inducing cell death. The above mechanisms may lead to endothelial injury and cardiotoxicity. CVD cardiovascular disease, CTR1 calcitonin receptor 1, DLAT dihydrolipoamide S-acetyltransferase, Fe-S iron-sulfur proteins, GSH glutathione, S sulfur ion, TCA tricarboxylic acid cycle. The figure was created with Figdraw (https://www.figdraw.com/).

Back to article page