The molecular mechanism of cuproptosis and research progress in pancreatic diseases.

In 30 seconds

This systematic review thematically analysed 113 publications identified through PubMed and Web of Science on cuproptosis mechanisms and their relevance to pancreatic diseases. It describes cuproptosis as copper accumulation associated with ferritin instability and aggregation of acylated proteins, leading to oxidative stress-related cell death. The reviewed literature links this process to pancreatic cancer, pancreatitis, diabetes, pancreatic cysts and injury, and pancreatic neuroendocrine tumours. The authors report that cuproptosis inducers alleviated pancreatic cancer in studies reviewed, whereas copper chelators promoted recovery from pancreatic injury by inhibiting cuproptosis.

Key findings

• The review included 113 key publications addressing cuproptosis mechanisms and pancreatic disease.
• Cuproptosis was linked in the reviewed literature to pancreatic cancer, acute and chronic pancreatitis, diabetes, pancreatic cysts and injury, and pancreatic neuroendocrine tumours.
• Disulfiram, chloroquinolones, and perilla phenols were reported to alleviate pancreatic cancer by promoting cuproptosis.
• Tetraethylenepentamine and tetrathiomolybdate were reported to promote recovery from pancreatic injury by inhibiting cuproptosis.

Why it matters

The review highlights that cuproptosis may have different implications across pancreatic conditions: promoting it was associated with benefit in pancreatic cancer, while inhibiting it was associated with recovery from pancreatic injury. This context-dependent pattern is relevant to interpreting copper-related mechanisms and underscores that therapeutic approaches would need to account for the disease being targeted.

What to keep in mind

The paper is a thematic review of existing literature; the abstract does not report a quantitative synthesis or clinical trial evidence.