AI Article Synopsis

  • Copper is vital for biological functions, but its regulation is key to preventing toxic effects; the study focuses on "cuproptosis," a form of cell death linked to copper excess.
  • Copper ionophores, such as elesclomol and disulfiram, raise intracellular copper levels, inducing oxidative stress and cell death, which could be leveraged for cancer therapies.
  • The research identifies potential biomarkers and therapeutic targets related to copper in cancer and copper-related diseases, suggesting new strategies for treatment in modern medicine.

Article Abstract

Copper, an essential element for various biological processes, demands precise regulation to avert detrimental health effects and potential cell toxicity. This paper explores the mechanisms of copper-induced cell death, known as cuproptosis, and its potential health and disease implications, including cancer therapy. Copper ionophores, such as elesclomol and disulfiram, increase intracellular copper levels. This elevation triggers oxidative stress and subsequent cell death, offering potential implications in cancer therapy. Additionally, copper ionophores disrupt mitochondrial respiration and protein lipoylation, further contributing to copper toxicity and cell death. Potential targets and biomarkers are identified, as copper can be targeted to those proteins to trigger cuproptosis. The role of copper in different cancers is discussed to understand targeted cancer therapies using copper nanomaterials, copper ionophores, and copper chelators. Furthermore, the role of copper is explored through diseases such as Wilson and Menkes disease to understand the physiological mechanisms of copper. Exploring cuproptosis presents an opportunity to improve treatments for copper-related disorders and various cancers, with the potential to bring significant advancements to modern medicine.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10854864PMC
http://dx.doi.org/10.3390/cancers16030647DOI Listing

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