Copper Homeostasis and Cuproptosis As Potential Intervention Strategy in Atherosclerosis

Area of Science:

• Biochemistry
• Molecular Biology
• Cardiovascular Research

Background:

• Atherosclerosis (AS) is a major cause of cardiovascular disease mortality, characterized by lipid accumulation and inflammation.
• Cellular dysfunction in AS is increasingly linked to copper (Cu) metabolism and cuproptosis, a regulated cell death pathway.
• Understanding the role of cuproptosis in AS pathogenesis is crucial for developing novel therapeutic interventions.

Purpose of the Study:

• To review the influence of proteins and signaling pathways regulating copper homeostasis and cuproptosis in AS.
• To explore potential therapeutic strategies targeting cuproptosis in AS.
• To discuss emerging treatments and future directions for translational medicine in AS.

Main Methods:

• Literature review focusing on copper homeostasis, cuproptosis, and atherosclerosis.
• Analysis of key regulatory proteins and signaling pathways involved in copper metabolism and cell death.
• Identification of potential therapeutic agents and strategies targeting cuproptosis.

Main Results:

• Cuproptosis significantly impacts cell function and survival within AS lesions through various downstream pathways.
• Key regulatory proteins and signaling pathways governing copper homeostasis are implicated in AS.
• Several therapeutic avenues, including endogenous metabolites, copper ionophores, nanoparticles, and natural products, show potential for targeting cuproptosis in AS.

Conclusions:

• Cuproptosis is a critical mechanism in AS pathogenesis, offering a novel therapeutic target.
• Modulating copper homeostasis and cuproptosis presents a promising strategy for AS treatment.
• Further research into targeted cuproptosis therapies holds potential for advancing cardiovascular medicine.