ArticleCytotechnology2025
Naringin regulates the cGAS-STING pathway to improve mitochondrial dysfunction and ferroptosis after myocardial ischemia-reperfusion injury.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Imbalance of the Regulated Cell Death and Autophagic Network: A Core Mechanism Driving Toxicological and Ischemic Myocardial Injury and a Target for Intervention with Traditional Chinese Medicine.Cardiovascular toxicology · 2026Review
- Potential Relationship Between Ferroptosis and Pyroptosis in Myocardial Ischemia/Reperfusion Injury: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- Baicalin Attenuates Oxidative Stress and Apoptosis in Myocardial Ischemia/reperfusion Injury via Suppression of STING/NLRP3 Pathway.Journal of cardiovascular translational research · 2026Article
- Cardioprotective effects of naringin, hesperidin, and hesperetin: modulation of atherosclerosis, cardiac remodeling, and myocardial ischemia/infarction.Frontiers in nutrition · 2026Review
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.Frontiers in immunology · 2026Review
- Interplay of cGAS-STING and ferroptosis: crosstalk, molecular mechanisms, and therapeutic prospects.Archives of toxicology · 2025Review
- Recent advances in the interaction of ferroptosis and immune-mediated inflammation in cardiovascular disease: mechanisms and therapeutic potential.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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