ArticleJournal of neurochemistry2013
Ischemic post-conditioning facilitates brain recovery after stroke by promoting Akt/mTOR activity in nude rats.
Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 70 citations in OpenAlex.
- Non-canonical role of "S6K1-SGK1" pathway in neuronal necroptosis following traumatic brain injury.Genes & diseases · 2026Article
- Noncanonical feedback loop between "RIP3-MLKL" and "4EBP1-eIF4E" promotes neuronal necroptosis.MedComm · 2025Article
- Reversing Persistent PTEN Activation after Traumatic Brain Injury Fuels Long-Term Axonal Regeneration via Akt/mTORC1 Signaling Cascade.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification of prognostic biomarkers of sepsis and construction of ceRNA regulatory networks.Scientific reports · 2025Article
- Ischemic Postconditioning Regulates New Cell Death Mechanisms in Stroke: Disulfidptosis.Biomolecules · 2024Article
- Neuroprotective effect of ischemic postconditioning against hyperperfusion and its mechanisms of neuroprotection.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2024Review
- Review
- Brain delivering RNA-based therapeutic strategies by targeting mTOR pathway for axon regeneration after central nervous system injury.Neural regeneration research · 2022Review
- Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration.Molecular neurodegeneration · 2021Review
- Advances in intervention methods and brain protection mechanisms of in situ and remote ischemic postconditioning.Metabolic brain disease · 2021Review
- p53 Inhibition Protects against Neuronal Ischemia/Reperfusion Injury by the p53/PRAS40/mTOR Pathway.Oxidative medicine and cellular longevity · 2021Article
- Article
- Luteolin Protects Against CIRI, Potentially via Regulation of the SIRT3/AMPK/mTOR Signaling Pathway.Neurochemical research · 2020Article
- Translation Regulation by eIF2α Phosphorylation and mTORC1 Signaling Pathways in Non-Communicable Diseases (NCDs).International journal of molecular sciences · 2020Review
- Ischemic postconditioning for stroke treatment: current experimental advances and future directions.Conditioning medicine · 2020Article
- Remote Postischemic Conditioning Promotes Stroke Recovery by Shifting Circulating Monocytes to CCR2The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Inhibition of the glutamine transporter SNAT1 confers neuroprotection in mice by modulating the mTOR-autophagy system.Communications biology · 2019Article
- Remote ischemic conditioning: a promising therapeutic intervention for multi-organ protection.Aging · 2018Article
- Hypoxia and Ischemia Promote a Maladaptive Platelet Phenotype.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Inhibition of mTOR protects the blood-brain barrier in models of Alzheimer's disease and vascular cognitive impairment.American journal of physiology. Heart and circulatory physiology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
While pre-conditioning is induced before stroke onset, ischemic post-conditioning (IPostC) is performed after reperfusion, which typically refers to a series of mechanical interruption of blood reperfusion after stroke. IPostC is known to reduce infarction in wild-type animals. We investigated if IPostC protects against brain injury induced by focal ischemia in Tcell-deficient nude rats and to examine its effects on Akt and the mammalian target of rapamycin (mTOR) pathway. Although IPostC reduced infarct size at 2 days post-stroke in wild-type rats, it did not attenuate infarction in nude rats. Despite the unaltered infarct size in nude rats, IPostC increased levels of phosphorylated Akt (p-Akt) and Akt isoforms (Akt1, Akt2, Akt3), and p-mTOR, p-S6K and p-4EBP1 in the mTOR pathway, as well as growth associated Protein 43 (GAP43), both in the peri-infarct area and core, 24 h after stroke. IPostC improved neurological function in nude rats 1-30 days after stroke and reduced the extent of brain damage 30 days after stroke. The mTOR inhibitor rapamycin abolished the long-term protective effects of IPostC. We determined that IPostC did not inhibit acute infarction in nude rats but did provide long-term protection by enhancing Akt and mTOR activity during the acute post-stroke phase. Post-conditioning did not attenuate infarction in nude rats measured 2 days post-stroke, but improved neurological function in nude rats and reduced brain damage 30 days after stroke. It resulted in increased-activities of Akt and mTOR, S6K and p-4EBP1. The mTOR inhibitor rapamycin abolished the long-term protective effects of IPostC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.