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<p>Copper ions are essential metal ions that play a pivotal role in various biochemical processes. Recent studies have identified a novel copper-dependent form of cell death named cuproptosis, which differs significantly from other well-characterized modes of cell death, such as apoptosis, pyroptosis, necrosis and ferroptosis. Moreover, a series of researches indicate that cuproptosis may be related to the occurrence and aggravation of cardiovascular diseases (CVDs). This review aims to elucidate the molecular mechanisms underlying cuproptosis and to summarize the pathways through which cuproptosis contributes to the pathogenesis of various cardiovascular conditions, including atherosclerosis, heart failure, dilated cardiomyopathy, atrial fibrillation, myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, acute myocardial infarction, and vascular aging. Additionally, we explore therapeutic approaches involving copper chelators, small-molecule inhibitors targeting copper chaperone proteins, and copper ionophores, which may mitigate these cardiovascular disorders by inhibiting cuproptosis. Collectively, effective suppression of cuproptosis may become a novel therapeutic strategy for the prevention and treatment of related CVDs.</p>

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Cuproptosis and Its Impact on Cardiovascular Health: Mechanisms and Therapeutic Opportunities

  • 期刊论文

  • 发表日期：

    2026年1月27日

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  • Xiaohui Huang,
  • Liwen Wang,
  • Huimei Liu,
  • Ruirui Lu,
  • Lanfang Li

摘要

Copper ions are essential metal ions that play a pivotal role in various biochemical processes. Recent studies have identified a novel copper-dependent form of cell death named cuproptosis, which differs significantly from other well-characterized modes of cell death, such as apoptosis, pyroptosis, necrosis and ferroptosis. Moreover, a series of researches indicate that cuproptosis may be related to the occurrence and aggravation of cardiovascular diseases (CVDs). This review aims to elucidate the molecular mechanisms underlying cuproptosis and to summarize the pathways through which cuproptosis contributes to the pathogenesis of various cardiovascular conditions, including atherosclerosis, heart failure, dilated cardiomyopathy, atrial fibrillation, myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, acute myocardial infarction, and vascular aging. Additionally, we explore therapeutic approaches involving copper chelators, small-molecule inhibitors targeting copper chaperone proteins, and copper ionophores, which may mitigate these cardiovascular disorders by inhibiting cuproptosis. Collectively, effective suppression of cuproptosis may become a novel therapeutic strategy for the prevention and treatment of related CVDs.