ArticleOxidative medicine and cellular longevity2021
The Protective Effect of Cyanidin-3-Glucoside on Myocardial Ischemia-Reperfusion Injury through Ferroptosis.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.
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Who cites it
81 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Mitochondrial dysfunction in cardiovascular disease: Towards exercise regulation of mitochondrial function.Frontiers in physiology · 2023Pooled it
- Unlocking the potential of deferoxamine: a systematic review on its efficacy and safety in alleviating myocardial ischemia-reperfusion injury in adult patients following cardiopulmonary bypass compared to standard care.Therapeutic advances in cardiovascular diseasePooled it
- Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026Review
- Ubiquitination-dependent regulation of ferroptosis in ischemic heart and brain.Redox biology · 2026Review
- Implications of ferritinophagy in cardiovascular diseases and its pharmacological modulation: underlying mechanisms and clinical translation strategies.Cellular & molecular biology letters · 2026Review
- Mechanisms of the RGS12-GPX4-ACSL4 signaling axis in regulating ferroptosis during myocardial ischemia-reperfusion injury.Journal of anesthesia and translational medicine · 2026Review
- miR-203 Alleviates Myocardial Damage Caused by Acute Coronary Syndrome by Inhibiting CA125.Biochemical genetics · 2026Article
- Dihydroorotate Dehydrogenase as a Modulator of Ferroptosis in Myocardial Ischemia-reperfusion Injury.Current molecular medicine · 2026Article
- Ferroptosis in Cardiovascular Diseases and Ferroptosis-Related Intervention Approaches.Cardiovascular drugs and therapy · 2025Review
- Self-assembled cyanidin-3-O-glucoside nanoparticles alleviate inflammation and ferroptosis induced by PRRSV infection.Journal of virology · 2025Article
- The interaction between ferroptosis and myocardial ischemia-reperfusion injury: molecular mechanisms and potential therapeutic targets.European journal of medical research · 2025Review
- Iron homeostasis and ferroptosis in muscle diseases and disorders: mechanisms and therapeutic prospects.Bone research · 2025Review
- Bee Pollen Potential to Modulate Ferroptosis: Phytochemical Insights for Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Validation and the role of PDK4 relevant to ferroptosis in degenerative lumbar disc disease.Journal of orthopaedic surgery and research · 2025Article
- Semaglutide attenuates myocardial ischemia-reperfusion injury by inhibiting ferroptosis of cardiomyocytes via activation of PKC-S100A9 axis.Frontiers in pharmacology · 2025Article
- Article
- Multi-omics approach to personalised treatment: insights into thrombus-derived exosome regulation in cardiomyocyte ferritinophagy.Frontiers in immunology · 2025Article
- Progress in the study of the mechanism of ferroptosis in coronary heart disease and clinical intervention strategies.Frontiers in cardiovascular medicine · 2025Review
- Natural flavonoids from herbs and nutraceuticals as ferroptosis inhibitors in central nervous system diseases: current preclinical evidence and future perspectives.Frontiers in pharmacology · 2025Review
- Astaxanthin mitigates doxorubicin-induced cardiotoxicity via inhibiting ferroptosis and autophagy: a study based on bioinformatic analysis andFrontiers in pharmacology · 2025Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was conducted to estimate the protective effect of Cyanidin-3-glucoside (C3G) on myocardial ischemia-reperfusion (IR) injury and to explore its mechanism. The rats were subjected to left anterior descending ligation and perfusion surgery. In vitro experiments were performed on H9c2 cells using the oxygen-glucose deprivation/reoxygenation (OGD/R) model. The results showed the administration of C3G reduced the infarction area, mitigated pathological alterations, inhibited ST segment elevation, and attenuated oxidative stress and ferroptosis-related protein expression. C3G also suppressed the expressions of USP19, Beclin1, NCOA4, and LC3II/LC3I. In addition, treatment with C3G relieved oxidative stress, downregulated LC3II/LC3I, reduced autophagosome number, downregulated TfR1 expression, and upregulated the expressions of FTH1 and GPX4 in OGD/R-induced H9c2 cells. C3G could inhibit the protein levels of USP19 and LC3II. C3G promoted K11-linked ubiquitination of Beclin1. Further evidence that C3G reduced ferroptosis and ameliorated myocardial I/R injury was demonstrated with the ferroptosis promoter RSL3. Taken together, C3G could be a potential agent to protect myocardium from myocardial I/R injury.
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