# Cuproptosis and Diabetic Osteoporosis: Mechanisms and Therapeutic Prospects

**Authors:** Shih-Yu Chen, Wanyi Chen, Ze Gao, Yan Cui, Xiaofeng Zhu

PMC · DOI: 10.3390/ijms27031307 · International Journal of Molecular Sciences · 2026-01-28

## TL;DR

This review explores how cuproptosis, a new type of cell death, may be linked to diabetic osteoporosis and offers new research directions.

## Contribution

The paper systematically connects cuproptosis with glucose and bone metabolism in the context of diabetic osteoporosis.

## Key findings

- Cuproptosis is associated with glucose and bone metabolism.
- Copper homeostasis plays a role in maintaining bone quality.
- Cuproptosis differs from other forms of cell death and involves copper accumulation.

## Abstract

Diabetic osteoporosis (DOP) is a metabolic bone disease characterized by abnormal bone tissue structure and reduced bone strength in patients with diabetes. Its pathogenesis is complex, involving multiple factors rather than a single cause, and has not yet been fully elucidated. Cuproptosis, a novel form of programmed cell death discovered in 2022, differs mechanistically from apoptosis, necroptosis, and ferroptosis. This process relies on the accumulation of intracellular copper ions and is closely associated with mitochondrial respiration. Studies have indicated that cuproptosis is intimately linked to glucose metabolism and bone metabolism. This review explores the role of copper homeostasis in maintaining glucose metabolism and bone quality and systematically elucidates the potential associations between cuproptosis and these processes from molecular, cellular, and pathophysiological perspectives, aiming to provide new insights and prospects for future research directions in diabetic osteoporosis.

## Full-text entities

- **Diseases:** diabetes (MESH:D003920), metabolic bone disease (MESH:D001851), DOP (MESH:D010024)
- **Chemicals:** copper (MESH:D003300), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12897738/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12897738/full.md

## References

122 references — full list in the complete paper: https://tomesphere.com/paper/PMC12897738/full.md

---
Source: https://tomesphere.com/paper/PMC12897738