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Copper’s dual role: unravelling the link between copper homeostasis, cuproptosis, and cardiovascular diseases

This graphic depicts the interplay between copper homeostasis and cuproptosis and their role in cardiovascular diseases. Copper is vital for cardiac mitochondrial function, while its dysregulation induces cuproptosis via Ferredoxin1 (FDX1) and lipoic acid synthase (LIAS). Cuproptosis is linked to myocardial ischemia/reperfusion injury, heart failure, atherosclerosis, and arrhythmias. Copper deficiency impacts atherosclerosis markers. Therapeutic interventions include copper chelators (e.g., ammonium tetrathiomolybdate), and oxidative phosphorylation inhibitors like elesclomol and copper ionophores (CuII(atsm), CuII(gtsm), and disulfiram). These interventions modulate intracellular copper, elevate NO, and reduce inflammatory cytokines, contributing to decreased cardiovascular diseases.

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Acknowledgements

Department of Biotechnology, School of Integrative Biology, Central University of Tamil Nadu, supported by the Department of Science and Technology (DST) under the Scheme “Fund for Improvement of S&T Infrastructure (FIST)”. The Ramalingaswami Re-entry Fellowship (D.O. NO. BT/HRD/35/02/2006) awarded (2021) supported to Dr. Rajesh Parsanathan, from the Department of Biotechnology (DBT), Ministry of Science & Technology, Govt. of India.

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Correspondence to Rajesh Parsanathan.

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Parsanathan, R. Copper’s dual role: unravelling the link between copper homeostasis, cuproptosis, and cardiovascular diseases. Hypertens Res 47, 1440–1442 (2024). https://doi.org/10.1038/s41440-024-01636-4

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