ArticleInternational journal of biological sciences2015
Inhibition of mTOR Pathway by Rapamycin Reduces Brain Damage in Rats Subjected to Transient Forebrain Ischemia.
Article in International journal of biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 60 citations in OpenAlex.
- The mTOR/Akt pathway is involved in regulating astrocyte growth and GLT-1 expression during cerebral ischemia-reperfusion.PloS one · 2026Article
- Mechanisms of SIRT1/SIRT3-mediated reduction of mitochondrial regeneration and inflammatory response in diabetic cerebral ischemia-reperfusion injury.Metabolic brain disease · 2025Article
- Neuroprotective Activities of Sertraline, Tiagabine, and Bicifadine with Autophagy-Inducing Potentials in a 6-Hydroxidopamine-Treated Parkinson's Disease Cell Model.Neurochemical research · 2025Article
- BNIP3-mediated mitophagy attenuates hypoxic-ischemic brain damage in neonatal rats by inhibiting ferroptosis through P62-KEAP1-NRF2 pathway activation to maintain iron and redox homeostasis.Acta pharmacologica Sinica · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- The Neuroprotective Effects of Caffeine in a Neonatal Hypoxia-Ischemia Model are Regulated through the AMPK/mTOR Pathway.International journal of biological sciences · 2025Article
- Progress in the study of the mechanism of ferroptosis in coronary heart disease and clinical intervention strategies.Frontiers in cardiovascular medicine · 2025Review
- Rapamycin Alleviates Neuronal Injury and Modulates Microglial Activation After Cerebral Ischemia.Molecular neurobiology · 2024Article
- Pharmacological inhibition of mTORC1 reduces neural death and damage volume after MCAO by modulating microglial reactivity.Biology direct · 2024Article
- LncRNA-HOTAIRM1 promotes aerobic glycolysis and proliferation in osteosarcoma via the miR-664b-3p/Rheb/mTOR pathway.Cancer science · 2023Article
- IGF/mTORC1/S6 Signaling Is Potentiated and Prolonged by Acute Loading of Subtoxicological Manganese Ion.Biomolecules · 2023Article
- Therapeutic modulation of JAK-STAT, mTOR, and PPAR-γ signaling in neurological dysfunctions.Journal of molecular medicine (Berlin, Germany) · 2023Review
- mTOR pathway - a potential therapeutic target in stroke.Therapeutic advances in neurological disorders · 2023Review
- Neurotrophic fragments as therapeutic alternatives to ameliorate brain aging.Neural regeneration research · 2023Review
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Possible Involvement of DNA Methylation in TSC1 Gene Expression in Neuroprotection Induced by Hypoxic Preconditioning.Oxidative medicine and cellular longevity · 2022Article
- Novel Therapeutic Strategies for Ischemic Stroke: Recent Insights into Autophagy.Oxidative medicine and cellular longevity · 2022Review
- Hyperglycemia aggravates ischemic brain damageFrontiers in endocrinology · 2022Article
- Lipid metabolism, inflammation, and foam cell formation in health and metabolic disorders: targeting mTORC1.Journal of molecular medicine (Berlin, Germany) · 2021Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aims of this study are to clarify the role of mTOR in mediating cerebral ischemic brain damage and the effects of rapamycin on ischemic outcomes. Ten minutes of forebrain ischemia was induced in rats, and their brains were sampled after 3 h, 16 h, and 7 days reperfusion for histology, immunohistochemistry and biochemical analysis. Our data demonstrated that cerebral ischemia resulted in both apoptotic and necrotic neuronal death; cerebral ischemia and reperfusion led to significant increases of mRNA and protein levels of p-mTOR and its downstream p-P70S6K and p-S6; elevation of LC3-II, and release of cytochrome c into the cytoplasm in both the cortex and hippocampus. Inhibition of mTOR by rapamycin markedly reduced ischemia-induced damage; suppressed p-Akt, p-mTOR, p-P70S6K and p-S6 protein levels; decreased LC3-II and Beclin-1; and prevented cytochrome c release in the two structures. All together, these data provide evidence that cerebral ischemia activates mTOR and autophagy pathways. Inhibition of mTOR deactivates the mTOR pathway, suppresses autophagy, prevents cytochrome c release and reduces ischemic brain damage.
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