Review shows cuproptosis influences pathogenesis and potential biomarkers in inflammatory bowel disease, suggesting new treatment strategies.
Inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease, is a common, recurring, chronic intestinal inflammatory illness that is considered to be impacted by the immune system, gut microbiota and genetic factors. Copper (Cu), a crucial metal ion in cuproptosis, contributes to IBD, with studies revealing that its dysregulation contributes to oxidative stress, intestinal inflammation, gut dysbiosis and disruption of barrier integrity. Additionally, cuproptosis‑related genes have been implicated in the pathogenesis of IBD, characterized by defects in barrier integrity and enhanced immune responses. These genes have been identified as biomarkers of IBD, providing novel therapeutic strategies for exploring their treatment. The present review highlights the mechanism of cuproptosis and the role of Cu in IBD. The review also highlights the cuproptosis‑related genes in the pathogenesis of IBD, as well as their applications as biomarkers for therapeutic purposes. These biomarkers may provide a reference for IBD for clinical decision‑making. The primary challenge is the lack of standard clinical medications for treating IBD associated with cuproptosis‑related genes. Consequently, researchers are employing molecular docking and other techniques to identify potential drugs aimed at these genes for therapeutic purposes.
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Chen et al. (2026) studied this question.
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