ArticleOxidative medicine and cellular longevity2021
Vitexin Mitigates Myocardial Ischemia/Reperfusion Injury in Rats by Regulating Mitochondrial Dysfunction via Epac1-Rap1 Signaling.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- TMC6 Protects Against Ischemic Neuronal Injury by Activating Rap1/Rac1 Signaling to Restore Mitochondrial Dynamics and Mitophagy.Molecular neurobiology · 2026Article
- Protective role of HOXB5-orchestrated mitochondrial homeostasis and mitophagy in cardiomyocytes after ischemia-reperfusion via transcriptionally activating Sirt5.Cardiovascular drugs and therapy · 2026Article
- Morusin attenuates myocardial ischemia/reperfusion injury by inhibiting ferroptosis via dual activation of the Nrf2/HO-1 pathway and mTORC1-dependent GPX4 synthesis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bridging tradition and modernity: mitochondrial dynamics as a Traditional Chinese Medicine therapeutic target in cardiovascular disease.Chinese medicine · 2026Review
- Role of Chinese Medicine in Addressing Myocardial Ischemia Reperfusion Injury: A Comprehensive Review.Chinese journal of integrative medicine · 2026Review
- Dietary Flavonoids Vitexin and Isovitexin: New Insights into Their Functional Roles in Human Health and Disease Prevention.International journal of molecular sciences · 2025Review
- Study on the Synergistic Effect of Klotho and KRAS on Reducing Ferroptosis After Myocardial Infarction by Regulating RAP1/ERK Signaling Pathway.Applied biochemistry and biotechnology · 2025Article
- Neuroprotective effect of resveratrol on Epac-1/Rap-1 signaling pathway in ischemic stroke rats.Frontiers in neuroscience · 2025Article
- Vitexin's Role in Colon Cancer Apoptosis: AMPK/mTOR Pathway Modulation Explored Through Experimental and Computational Approaches.Recent patents on anti-cancer drug discovery · 2025Article
- Comprehensive evaluation of non-coding RNA-mediated autophagy regulation in myocardial ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Article
- Cepharanthine inhibits migration, invasion, and EMT of bladder cancer cells by activating the Rap1 signaling pathway in vitro.American journal of translational research · 2024Article
- The important role of miR-1-3p in cancers.Journal of translational medicine · 2023Review
- Host cell cAMP-Epac-Rap1b pathway inhibition by hawthorn extract as a potential target againstFrontiers in microbiology · 2023Article
- Dexmedetomidine Can Enhance PINK1/Parkin-Mediated Mitophagy in MPTP-Induced PD Mice Model by Activating AMPK.Oxidative medicine and cellular longevity · 2022Article
- Exploration of the regulatory mechanisms of regeneration, anti-oxidation, anti-aging and the immune response at the post-molt stage ofFrontiers in physiology · 2022Article
- Research progress on effects of traditional Chinese medicine on myocardial ischemia-reperfusion injury: A review.Frontiers in pharmacology · 2022Review
- Epac: A Promising Therapeutic Target for Vascular Diseases: A Review.Frontiers in pharmacology · 2022Review
- Proteomics Revealed That Mitochondrial Function Contributed to the Protective Effect of Herba Siegesbeckiae Against Cardiac Ischemia/Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
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Abstract
Revascularization is an effective therapy for rescuing myocardial tissue after ischemic events. However, the process of reperfusion can lead to more severe cardiomyocyte damage, called myocardial ischemia-reperfusion (I/R) injury (MIRI). We have previously shown that vitexin (VT) (a flavonoid compound derived from natural products) protects against MIRI; however, the exact mechanisms underpinning this effect require further elucidation. This study is aimed at elucidating the protective mechanism of VT in inhibiting ischemic myocardial mitochondrial dysfunction and reducing cardiomyocyte apoptosis by regulating Epac1-Rap1 signaling. Isolated rat hearts were subjected to MIRI in a Langendorff perfusion system, and H9c2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro. Our analyses show that during I/R, Epac1 expression was upregulated, left ventricular dysfunction deteriorated, mitochondrial dynamics were disrupted, and both myocardial cells and tissues exhibited apoptosis. Furthermore, administration of 8-CPT (an Epac agonist) exacerbated cardiomyocyte injury and mitochondrial dysfunction. Interestingly, suppressing the function of Epac1 through VT or ESI-09 (an Epac inhibitor) treatment during I/R reduced the myocardial infarct size, cardiomyocyte apoptosis, and reactive oxygen species production; alleviated mitochondrial dysfunction by increasing mitochondrial membrane potential; elevated MFN2 expression; and inhibited Drp1 expression. To our knowledge, our results reveal, for the first time, the mechanisms underlying the protective effect of VT in the myocardium of rats with MIRI. Moreover, we provide a new target and theoretical basis for VT in the treatment of ischemic heart disease.
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