ArticleOxidative medicine and cellular longevity2017
Reperfusion Therapy with Rapamycin Attenuates Myocardial Infarction through Activation of AKT and ERK.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- The clinical effect of nicorandil on perioperative myocardial protection in patients undergoing elective PCI: A Systematic Review and Meta-Analysis.Scientific reports · 2017Pooled it
- P2X4 receptor limits adverse cardiac remodeling following ischemia-reperfusion through regulation of autophagy in cardiac fibroblasts.Cell communication and signaling : CCS · 2026Article
- Melatonin and mitochondrial protection in cardiac ischemia-reperfusion injury: mechanisms, evidence and translational perspectives.Basic research in cardiology · 2026Review
- Macrophages lacking TSC2 have mTORC1-dependent increased GPNMB and ameliorate ventricular dysfunction/remodeling after ischemia-reperfusion.Scientific reports · 2025Article
- Anti-ageing interventions for the treatment of cardiovascular disease.Cardiovascular research · 2025Review
- High-density lipoprotein protects normotensive and hypertensive rats against ischemia-reperfusion injury through differential regulation of mTORC1 and mTORC2 signaling.Frontiers in pharmacology · 2024Article
- Single-Dose Treatment with Rapamycin Preserves Post-Ischemic Cardiac Function through Attenuation of Fibrosis and Inflammation in Diabetic Rabbit.International journal of molecular sciences · 2023Article
- Rapamycin Alternatively Modifies Mitochondrial Dynamics in Dendritic Cells to Reduce Kidney Ischemic Reperfusion Injury.International journal of molecular sciences · 2021Article
- CircRNA 010567 plays a significant role in myocardial infarction via the regulation of the miRNA-141/DAPK1 axis.Journal of thoracic disease · 2021Article
- Constitutive activation of ERK1/2 signaling protects against myocardial ischemia via inhibition of mitochondrial fragmentation in the aging heart.Annals of translational medicine · 2021Article
- Short- and long-term effects of rapamycin on ischemic damage and apoptotic changes in torsion of rat testes.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Differential Regulation of mTOR Complexes with miR-302a Attenuates Myocardial Reperfusion Injury in Diabetes.iScience · 2020Article
- Rapamycin inhibits AR signaling pathway in prostate cancer by interacting with the FK1 domain of FKBP51.Biochemistry and biophysics reports · 2020Article
- PDRPS7 protects cardiac cells from hypoxia/reoxygenation injury through inactivation of JNKs.FEBS open bio · 2020Article
- Mitochondrial Quality Control: Role in Cardiac Models of Lethal Ischemia-Reperfusion Injury.Cells · 2020Review
- Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3Oxidative medicine and cellular longevity · 2020Article
- HMGB1 promotes bone fracture healing through activation of ERK signaling pathway in a rat tibial fracture model.The Kaohsiung journal of medical sciences · 2019Article
- Spermidine-enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway.British journal of pharmacology · 2019Article
- α7nAChR Deletion Aggravates Myocardial Infarction and Enhances Systemic Inflammatory Reaction via mTOR-Signaling-Related Autophagy.Inflammation · 2019Article
- Snapshot: Implications for mTOR in Aging-related Ischemia/Reperfusion Injury.Aging and disease · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Prompt coronary reperfusion is the gold standard for minimizing injury following acute myocardial infarction. Rapamycin, mammalian target of Rapamycin (mTOR) inhibitor, exerts preconditioning-like cardioprotective effects against ischemia/reperfusion (I/R) injury. We hypothesized that Rapamycin, given at the onset of reperfusion, reduces myocardial infarct size through modulation of mTOR complexes. Adult C57 male mice were subjected to 30 min of myocardial ischemia followed by reperfusion for 1 hour/24 hours. Rapamycin (0.25 mg/kg) or DMSO (7.5%) was injected intracardially at the onset of reperfusion. Post-I/R survival (87%) and cardiac function (fractional shortening, FS: 28.63 ± 3.01%) were improved in Rapamycin-treated mice compared to DMSO (survival: 63%, FS: 17.4 ± 2.6%). Rapamycin caused significant reduction in myocardial infarct size (IS: 26.2 ± 2.2%) and apoptosis (2.87 ± 0.64%) as compared to DMSO-treated mice (IS: 47.0 ± 2.3%; apoptosis: 7.39 ± 0.81%). Rapamycin induced phosphorylation of AKT S473 (target of mTORC2) but abolished ribosomal protein S6 phosphorylation (target of mTORC1) after I/R. Rapamycin induced phosphorylation of ERK1/2 but inhibited p38 phosphorylation. Infarct-limiting effect of Rapamycin was abolished with ERK inhibitor, PD98059. Rapamycin also attenuated Bax and increased Bcl-2/Bax ratio. These results suggest that reperfusion therapy with Rapamycin protects the heart against I/R injury by selective activation of mTORC2 and ERK with concurrent inhibition of mTORC1 and p38.
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Registered trials
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