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<p>Myocardial ischemia/reperfusion (I/R) injury is a major global health problem with high rates of mortality and disability, which is more severe in patients with diabetes. Substantial researches have documented that diabetic myocardium are more susceptible to I/R injury, but many current intervention strategies against myocardial I/R injury have limited effectiveness in diabetic hearts. Caveolin-3 (Cav-3) is the signature protein of caveolae and serves as a signal integration and transduction platform in the plasma membrane of cardiomyocytes, which plays a vital role in myocardial functions, metabolism and protection of multiple conditioning strategies against I/R injury. Nevertheless, numerous studies have revealed that the expression of Cav-3 is impaired in diabetic hearts, which contributes to increased vulnerability of myocardium to I/R injury and resistance to protective conditioning strategies. In this review, we outline the basic structure and function of Cav-3, emphatically present the unique role of Cav-3 as a signal integration and transduction element in diabetic myocardial I/R injury and discuss its therapeutic perspective in strategies against myocardial I/R injury in diabetes.</p>

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Caveolin-3: therapeutic target for diabetic myocardial ischemia/reperfusion injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月26日

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  • Xinyu Wen,
  • Yanwei Ji,
  • Hepeng Tang,
  • Zhenshuai Jin,
  • Wating Su,
  • Lu Zhou,
  • Zhong-Yuan Xia,
  • Lin Li,
  • Shaoqing Lei

摘要

Myocardial ischemia/reperfusion (I/R) injury is a major global health problem with high rates of mortality and disability, which is more severe in patients with diabetes. Substantial researches have documented that diabetic myocardium are more susceptible to I/R injury, but many current intervention strategies against myocardial I/R injury have limited effectiveness in diabetic hearts. Caveolin-3 (Cav-3) is the signature protein of caveolae and serves as a signal integration and transduction platform in the plasma membrane of cardiomyocytes, which plays a vital role in myocardial functions, metabolism and protection of multiple conditioning strategies against I/R injury. Nevertheless, numerous studies have revealed that the expression of Cav-3 is impaired in diabetic hearts, which contributes to increased vulnerability of myocardium to I/R injury and resistance to protective conditioning strategies. In this review, we outline the basic structure and function of Cav-3, emphatically present the unique role of Cav-3 as a signal integration and transduction element in diabetic myocardial I/R injury and discuss its therapeutic perspective in strategies against myocardial I/R injury in diabetes.