2 weeks Ago
Atherosclerosis (AS) is a chronic inflammatory disease characterized by the buildup of lipids and immune cells in arterial walls, increasing the risk of cardiovascular conditions. While multiple factors contribute to AS, recent research highlights the role of copper, an essential trace element, in disease progression. Copper plays a crucial role in mitochondrial function, oxidative stress regulation, and vascular health.
However, excess copper can become toxic, triggering oxidative damage and inflammation—two key drivers of AS. A newly identified form of regulated cell death, known as cuproptosis, may be a critical mechanism linking copper imbalance to vascular damage. The research is published in the journal Biomolecules and Biomedicine .
Cuproptosis is a unique, copper-dependent form of cell death that differs from apoptosis and necrosis. It occurs when intracellular copper binds to proteins involved in the tricarboxylic acid (TCA) cycle, leading to protein aggregation, mitochondrial dysfunction, and ultimately, cell death. This discovery underscores the importance of copper homeostasis in maintaining vascular health.
Several mechanisms explain how cuproptosis may drive AS progression: Given these mechanisms, targeting cuproptosis could open new avenues for AS treatment and prevention. Recent studies have identified key cuproptosis-related biomarkers that could aid in early AS detection and intervention: These biomarkers may serve as diagnostic tools, enabling earlier detection and targeted therapies for AS. Several strategies are being explored to regulate copper levels and mitigate cuproptosis-related damage in AS: While cuproptosis represents a promising target for AS treatment, several challenges remain: By addressing these challenges, researchers aim to develop more effective, targeted treatments for AS, improving cardiovascular health and reducing disease burden.
More information: Jiankang Wang et al, The molecular mechanisms of cuproptosis and its relevance to atherosclerosis, Biomolecules and Biomedicine (2025). DOI: 10.17305/bb.
2024.11826.
