Copper Metabolism and Cardiovascular Health

Copper is an essential trace element that serves as a catalytic cofactor in key enzymatic processes, including mitochondrial respiration, antioxidant defence and connective tissue crosslinking. Physiological copper levels are maintained through coordinated actions of membrane transporters, such as CTR1 and ATP7A/B, and intracellular copper chaperones, which deliver copper ions safely to target enzymes. Both copper deficiency and excess are implicated in cardiovascular pathology: insufficient copper impairs cytochrome c oxidase and superoxide dismutase activities, leading to energetic failure and oxidative stress in the myocardium, whereas copper overload promotes reactive oxygen species formation and inflammatory injury in vascular cells. Genetic disorders of copper regulation—Menkes disease and Wilson’s disease—illustrate the extremes of copper imbalance and its systemic consequences. Recent advances have identified a novel copper-dependent cell-death pathway, termed cuproptosis, linking mitochondrial protein aggregation to vascular dysfunction and plaque instability. Dietary variation in copper intake further modulates endothelial function and stroke risk on a population level. These insights into copper homeostasis and its disruption in cardiovascular tissues open avenues for biomarker development and tailored therapeutic strategies aimed at restoring copper balance and reducing the global burden of cardiovascular disease.

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Copper Metabolism and Cardiovascular Health publication trend

The graph below shows the total number of articles in copper metabolism and cardiovascular health across all publications each year (not limited to Nature Index journals).

Technical terms

Cuproptosis: A copper-dependent form of regulated cell death involving mitochondrial enzyme aggregation and proteotoxic stress.
Copper homeostasis: The coordinated control of copper absorption, distribution, utilisation and excretion to maintain physiological levels.
Copper chaperones: Intracellular proteins that bind and safely transport copper ions to specific enzyme targets.
Ceruloplasmin: The primary copper-carrying protein in plasma, involved in iron metabolism and antioxidant defence.
Ischaemia–reperfusion: Tissue injury caused when blood supply returns after a period of oxygen deprivation, often exacerbated by oxidative stress.

References

1. Copper homeostasis and copper-induced cell death in the pathogenesis of cardiovascular disease and therapeutic strategies. Cell Death & Disease (2023).
2. An Emerging Role of Defective Copper Metabolism in Heart Disease. Nutrients (2022).
3. Dietary Copper Intake and Risk of Stroke in Adults: A Case-Control Study Based on National Health and Nutrition Examination Survey 2013–2018. Nutrients (2022).