ReviewFrontiers in neuroscience2018
Role of mTORC1 Controlling Proteostasis after Brain Ischemia.
Review in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- Mitochondria as a therapeutic target in neurodegeneration caused by hypoxia and ischemia during the perinatal period.Pharmacological reports : PR · 2026Review
- Acute liver failure-induced arginine deficiency impairs blood-brain barrier via inhibiting mTORC1-S6K1/4EBP1 pathway and inducing autophagy.Cell death & disease · 2025Article
- Sirtuins Contribute to the Migraine-Stroke Connection.International journal of molecular sciences · 2025Review
- Targeting autophagy in astrocytes: a potential for neurodegenerative disease intervention.Frontiers in cellular neuroscience · 2025Review
- Autophagy-mediated regulation of neutrophil inflammatory responses and its relevance to central nervous system diseases.Frontiers in aging neuroscience · 2025Review
- Blood-brain barrier repair: potential and challenges of stem cells and exosomes in stroke treatment.Frontiers in cellular neuroscience · 2025Review
- Exploring research trends and hotspots in PI3K/Akt signaling pathway in ischemic stroke: a bibliometric analysis.Frontiers in molecular neuroscience · 2025Article
- Activation of the LKB1/AMPK/HIF-1α Pathway by Metformin to Promote Neovascularisation in Cerebral Ischaemia.Neurochemical research · 2024Article
- Pharmacological inhibition of mTORC1 reduces neural death and damage volume after MCAO by modulating microglial reactivity.Biology direct · 2024Article
- Hexahydrocurcumin attenuated demyelination and improved cognitive impairment in chronic cerebral hypoperfusion rats.Inflammopharmacology · 2024Article
- Article
- Role of autophagy in ischemic stroke: insights from animal models and preliminary evidence in the human disease.Frontiers in cell and developmental biology · 2024Review
- Sex-biased autophagy as a potential mechanism mediating sex differences in ischemic stroke outcome.Neural regeneration research · 2023Review
- eEF1A2 siRNA Suppresses MPPTheScientificWorldJournal · 2023Article
- Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022Review
- Dysregulation of mTOR Signaling after Brain Ischemia.International journal of molecular sciences · 2022Review
- Research progress on astrocyte autophagy in ischemic stroke.Frontiers in neurology · 2022Review
- Neferine Protects Against Brain Damage in Permanent Cerebral Ischemic Rat Associated with Autophagy Suppression and AMPK/mTOR Regulation.Molecular neurobiology · 2021Article
- A 3R-Tau-mediated mechanism in oligodendrocytes: could it be the key for neuroprotection after stroke?Neural regeneration research · 2021Review
- Dexamethasone Protects Against Ischaemic Brain Injury via Inhibiting the pAkt Signalling Pathway Through Increasing Hap1.Neurotoxicity research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intense efforts are being undertaken to understand the pathophysiological mechanisms triggered after brain ischemia and to develop effective pharmacological treatments. However, the underlying molecular mechanisms are complex and not completely understood. One of the main problems is the fact that the ischemic damage is time-dependent and ranges from negligible to massive, involving different cell types such as neurons, astrocytes, microglia, endothelial cells, and some blood-derived cells (neutrophils, lymphocytes, etc.). Thus, approaching such a complicated cellular response generates a more complex combination of molecular mechanisms, in which cell death, cellular damage, stress and repair are intermixed. For this reason, animal and cellular model systems are needed in order to dissect and clarify which molecular mechanisms have to be promoted and/or blocked. Brain ischemia may be analyzed from two different perspectives: that of oxygen deprivation (hypoxic damage
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What OpenQuestion holds
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.