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<p>Diabetes with myocardial ischemia-reperfusion injury(MIRI) represents a common complication of diabetes mellitus (DM), and cardiovascular disease remains the leading cause of death in DM patients. Consequently, preventing cardiovascular disease in individuals with diabetes continues to pose a significant challenge. Hyperglycemia-induced elevation of reactive oxygen species (ROS), activation of ferroptosis, and impairment of cardioprotective pathways collectively increase diabetic patients’ susceptibility to myocardial ischemia. MIRI, characterized by oxygen deprivation followed by restoration of blood flow, causes irreversible tissue damage. The pathophysiological mechanisms underlying MIRI in diabetes involve ferroptosis, oxidative stress, inflammation, intracellular calcium overload, and endoplasmic reticulum stress. These mechanisms interact synergistically to directly or indirectly aggravate myocardial damage. This review aims to achieve two objectives:&#xa0;first, to summarize the underlying pathogenic mechanisms of MIRI in DM; second, to outline the pharmacological effects and molecular targets of therapeutic agents for diabetic MIRI.</p>

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Myocardial ischemia reperfusion in diabetes: mechanism of injury and its drug treatment

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月31日

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  • Pei Han Duan,
  • Hong Xin Li,
  • Jian Hui Li,
  • Li Ping Xing,
  • An Nan Liu,
  • Chen Hui Wang,
  • Kong Fei

摘要

Diabetes with myocardial ischemia-reperfusion injury(MIRI) represents a common complication of diabetes mellitus (DM), and cardiovascular disease remains the leading cause of death in DM patients. Consequently, preventing cardiovascular disease in individuals with diabetes continues to pose a significant challenge. Hyperglycemia-induced elevation of reactive oxygen species (ROS), activation of ferroptosis, and impairment of cardioprotective pathways collectively increase diabetic patients’ susceptibility to myocardial ischemia. MIRI, characterized by oxygen deprivation followed by restoration of blood flow, causes irreversible tissue damage. The pathophysiological mechanisms underlying MIRI in diabetes involve ferroptosis, oxidative stress, inflammation, intracellular calcium overload, and endoplasmic reticulum stress. These mechanisms interact synergistically to directly or indirectly aggravate myocardial damage. This review aims to achieve two objectives: first, to summarize the underlying pathogenic mechanisms of MIRI in DM; second, to outline the pharmacological effects and molecular targets of therapeutic agents for diabetic MIRI.