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<p>Myocardial ischemia–reperfusion injury (MI/RI) is a crucial complication of reperfusion treatment for myocardial infarction. Naringin (Nar) is a flavonoid with identified cardioprotective functions. This study aimed to explore the protective mechanisms of Nar against MI/RI, specifically focusing on its modulation of the cGAS-STING pathway. An H9c2 cardiomyocyte hypoxia/reoxygenation (H/R) injury model and an MI/R rat model were established. Our findings demonstrated that Nar, at a concentration of 480&#xa0;μM, exhibited no cytotoxic effects on H9c2 cardiomyocytes and did not inhibit cell proliferation. Nar significantly reduced myocardial cell injury by improving mitochondrial function and decreasing oxidative stress, particularly the stress induced by a ferroptosis activator (Erastin). Additionally, the in vivo MI/R rat model further confirmed that Nar inhibited the activation of the cGAS-STING pathway, thereby attenuating myocardial injury. Collectively, Nar exerts protective effects against MI/RI by regulating mitochondrial dysfunction and ferroptosis, primarily through inhibition of the cGAS-STING pathway.</p>

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Naringin regulates the cGAS-STING pathway to improve mitochondrial dysfunction and ferroptosis after myocardial ischemia–reperfusion injury

  • 期刊论文

  • 发表日期：

    2025年5月16日

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  • Xinwei Zhang,
  • Junjie He,
  • Zhen Xu,
  • Yanna Yang

摘要

Myocardial ischemia–reperfusion injury (MI/RI) is a crucial complication of reperfusion treatment for myocardial infarction. Naringin (Nar) is a flavonoid with identified cardioprotective functions. This study aimed to explore the protective mechanisms of Nar against MI/RI, specifically focusing on its modulation of the cGAS-STING pathway. An H9c2 cardiomyocyte hypoxia/reoxygenation (H/R) injury model and an MI/R rat model were established. Our findings demonstrated that Nar, at a concentration of 480 μM, exhibited no cytotoxic effects on H9c2 cardiomyocytes and did not inhibit cell proliferation. Nar significantly reduced myocardial cell injury by improving mitochondrial function and decreasing oxidative stress, particularly the stress induced by a ferroptosis activator (Erastin). Additionally, the in vivo MI/R rat model further confirmed that Nar inhibited the activation of the cGAS-STING pathway, thereby attenuating myocardial injury. Collectively, Nar exerts protective effects against MI/RI by regulating mitochondrial dysfunction and ferroptosis, primarily through inhibition of the cGAS-STING pathway.