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Cuproptosis and copper deficiency in ischemic vascular injury and repair
Jiayi Gu1, Wei Huang1, Zheng Duanmu2
1Department of Neurology, The Fourth Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Insights
Copper
Area of Science:
- Biochemistry
- Vascular Biology
- Pathophysiology
Background:
- Ischemic vascular diseases are a growing global health concern.
- Copper plays a dual role in vascular health: deficiency increases risk, while excess causes injury.
- Cuproptosis, a copper-dependent cell death, is implicated in vascular damage.
Purpose of the Study:
- To review the role of copper and cuproptosis in ischemic injury and repair.
- To explore the impact of copper deficiency and excess on myocardial, cerebral, and limb ischemia.
- To discuss therapeutic strategies related to copper biology in ischemic vascular diseases.
Main Methods:
- Literature review of studies on copper metabolism and ischemic vascular diseases.
- Analysis of signaling pathways involved in copper-induced cytotoxicity and cell death.
- Synthesis of current understanding of copper's role in different types of ischemia.
Main Results:
- Copper deficiency impairs vascular elasticity and promotes platelet aggregation.
- Excess copper ions induce cytotoxicity and vascular injury via specific signaling pathways.
- Cuproptosis is a significant factor in the pathogenesis of ischemic conditions.
Conclusions:
- Copper homeostasis is critical for preventing and managing ischemic vascular diseases.
- Targeting copper metabolism offers potential therapeutic avenues for ischemic conditions.
- Further research into copper biology is essential for understanding ischemic disease mechanisms.
Abstract:
Ischemic vascular diseases are on the rise globally, including ischemic heart diseases, ischemic cerebrovascular diseases, and ischemic peripheral arterial diseases, posing a significant threat to life. Copper is an essential element in various biological processes, copper deficiency can reduce blood vessel elasticity and increase platelet aggregation, thereby increasing the risk of ischemic vascular disease; however, excess copper ions can lead to cytotoxicity, trigger cell death, and ultimately result in vascular injury through several signaling pathways. Herein, we review the role of cuproptosis and copper deficiency implicated in ischemic injury and repair including myocardial, cerebral, and limb ischemia. We conclude with a perspective on the therapeutic opportunities and future challenges of copper biology in understanding the pathogenesis of ischemic vascular disease states.
