ArticleNeurochemical research2019
MicroRNA-26b/PTEN Signaling Pathway Mediates Glycine-Induced Neuroprotection in SAH Injury.
Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Blockade of IRE1-XBP1 Signaling Pathway Ameliorates IL-6-dependent Nerve Damage and Neuron Pyroptosis after Subarachnoid Hemorrhage in Mice.Experimental neurobiology · 2026Article
- Metabolome Wide Mendelian Randomization Assessing the Causal Relationship Between Serum Metabolites, Cerebrospinal Metabolites, and Aneurysmal Subarachnoid Hemorrhage.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Hydroxymethyltransferase 2 promotes the development of glioblastoma by mediating WTAP regulation of PTEN N6-methyladenosine modification.Metabolic brain disease · 2025Article
- Src dependency of the regulation of LTP by alternative splicing ofPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Glycine-induced NMDA receptor internalization provides neuroprotection and preserves vasculature following ischemic stroke.iScience · 2022Article
- Noncoding RNA as Diagnostic and Prognostic Biomarkers in Cerebrovascular Disease.Oxidative medicine and cellular longevity · 2022Review
- MiR-499a prevents astrocytes mediated inflammation in ischemic stroke by targeting PTEN.Non-coding RNA research · 2021Article
- Peri-tumoral brain edema associated with glioblastoma correlates with tumor recurrence.Journal of Cancer · 2021Article
- Glycinergic Signaling in Macrophages and Its Application in Macrophage-Associated Diseases.Frontiers in immunology · 2021Review
- Epigenetic Regulations of Microglia/Macrophage Polarization in Ischemic Stroke.Frontiers in molecular neuroscience · 2021Review
- MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN.Bioscience reports · 2020Article
- Dexmedetomidine had neuroprotective effects on hippocampal neuronal cells via targeting lncRNA SHNG16 mediated microRNA-10b-5p/BDNF axis.Molecular and cellular biochemistry · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
Subarachnoid hemorrhage (SAH) is a form of stroke associated with high mortality and morbidity. Despite advances in treatment for SAH, the prognosis remains poor. We have previously demonstrated that glycine, a non-essential amino acid is involved in neuroprotection following intracerebral hemorrhage via the Phosphatase and tensin homolog (PTEN)/protein kinase B (AKT) signaling pathway. However, whether it has a role in inducing neuroprotection in SAH is not known. The present study was designed to investigate the role of glycine in SAH. In this study, we show that glycine can reduce brain edema and protect neurons in SAH via a novel pathway. Following a hemorrhagic episode, there is evidence of downregulation of S473 phosphorylation of AKT (p-AKT), and this can be reversed with glycine treatment. We also found that administration of glycine can reduce neuronal cell death in SAH by activating the AKT pathway. Glycine was shown to upregulate miRNA-26b, which led to PTEN downregulation followed by AKT activation, resulting in inhibition of neuronal death. Inhibition of miRNA-26b, PTEN or AKT activation suppressed the neuroprotective effects of glycine. Glycine treatment also suppressed SAH-induced M1 microglial polarization and thereby inflammation. Taken together, we conclude that glycine has neuroprotective effects in SAH and is mediated by the miRNA-26b/PTEN/AKT signaling pathway, which may be a therapeutic target for treatment of SAH injury.
Indexed as
Identifiers
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.