ArticleMolecular medicine reports2018
(‑)‑Epicatechin protects against myocardial ischemia‑induced cardiac injury via activation of the PTEN/PI3K/AKT pathway.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Tnxb Alleviates Myocardial Ischemia-Reperfusion Injury Through Facilitating Akt-Dependent Endothelial Cell Survival and Angiogenesis in Mice.Cardiovascular toxicology · 2026Article
- Role of natural products in cardiovascular disease.Molecular and cellular biochemistry · 2025Review
- Protective Role of (-)-Epicatechin on Trimethylamine-N-Oxide (TMAO)-Induced Cardiac Hypertrophy via SP1/SIRT1/SUMO1 Signaling Pathway.Cardiovascular toxicology · 2024Article
- Pharmacological Treatments and Therapeutic Targets in Muscle Dystrophies Generated by Alterations in Dystrophin-Associated Proteins.Medicina (Kaunas, Lithuania) · 2024Review
- Green tea catechin prevents oxidative stress-regulated autophagy and apoptosis signaling, and inhibits tenderness in postmortem bovineFood chemistry: X · 2023Article
- Small ubiquitin-related modifier (SUMO)ylation of SIRT1 mediates (-)-epicatechin inhibited- differentiation of cardiac fibroblasts into myofibroblasts.Pharmaceutical biology · 2022Article
- Supplementation with a Cocoa-Carob Blend, Alone or in Combination with Metformin, Attenuates Diabetic Cardiomyopathy, Cardiac Oxidative Stress and Inflammation in Zucker Diabetic Rats.Antioxidants (Basel, Switzerland) · 2022Article
- miRNA-425-5p enhances diffuse large B cell lymphoma growth by targeting PTEN.Translational cancer research · 2021Article
- Pharmacology of Catechins in Ischemia-Reperfusion Injury of the Heart.Antioxidants (Basel, Switzerland) · 2021Review
- Boosting Akt Pathway by Rupatadine Modulates Th17/Tregs Balance for Attenuation of Isoproterenol-Induced Heart Failure in Rats.Frontiers in pharmacology · 2021Article
- Tissue mechanics and expression of TROP2 in oral squamous cell carcinoma with varying differentiation.BMC cancer · 2020Article
- miRNA-425-5p enhances lung cancer growth via the PTEN/PI3K/AKT signaling axis.BMC pulmonary medicine · 2020Article
- TROP2 increases growth and metastasis of human oral squamous cell carcinoma through activation of the PI3K/Akt signaling pathway.International journal of molecular medicine · 2019Article
- Effects and Mechanisms of Tea and Its Bioactive Compounds for the Prevention and Treatment of Cardiovascular Diseases: An Updated Review.Antioxidants (Basel, Switzerland) · 2019Review
- Article
Corrections and comments
- Retracted
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Flavonol (‑)‑epicatechin (EPI) is primarily contained in green tea (Camellia sinensis) and cocoa beans (Theobroma cacao), and has been demonstrated to be beneficial for the health of the cardiovascular system. However, the effect and the underlying mechanism of EPI on myocardial ischemia induced cardiac injury has not yet been determined. Therefore, the present study aimed to detect whether EPI inhibited myocardial ischemia injury. An in vivo mouse myocardial ischemia model was induced by the ligation of left descending coronary artery for 7 days. EPI (1 mg/kg/day) was administrated 10 days prior to myocardial ischemia operation. The in vitro mouse myocardial ischemia model was induced by cultivating neonatal mouse cardiomyocytes under anoxia condition for 12 h. Cardiomyocytes were treated with EPI (5 µM) for 1 h and then incubated under anoxia conditions. Mouse hearts and cultured cardiomyocytes were used for hematoxylin‑eosin, masson, ultrasonography, terminal dUTP nick end‑labeling, immunofluorescence, western blotting and MTT assays. Results revealed that myocardial ischemia‑induced mouse cardiac injury was significantly inhibited by EPI, as evidenced by decreased myocardial apoptosis, cardiac fibrosis and myocardial hypertrophy and improved cardiac function. In addition, it was confirmed that EPI serves a protective effect against myocardial ischemia via the phosphatase and tensin homolog (PTEN)/phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway, which was reversed by the PI3K inhibitor, LY294002. The protective role of EPI in myocardial apoptosis was further confirmed on mouse cardiomyocytes following anoxia treatment in vitro. In conclusion, the data suggested that EPI protects against myocardial ischemia induced cardiac injury through the PTEN/PI3K/AKT signaling pathway in vivo and in vitro, which may provide clinical therapeutic approaches and targets for cardiac ischemia injury.
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