ArticleEMBO molecular medicine2024
Diabetes drugs activate neuroprotective pathways in models of neonatal hypoxic-ischemic encephalopathy.
Article in EMBO molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Semaglutide exerts neuroprotective effects by blocking the interleukin-17/NOD-like receptor family pyrin domain containing 3-mediated neuroinflammation pathway after traumatic brain injury.Neural regeneration research · 2026Article
- Exendin-4 improves neurodevelopmental outcome after neonatal germinal matrix hemorrhage.Cell death & disease · 2026Article
- Converging neurotrophic-immune signaling in autism spectrum disorder: integrative roles of klotho, GDNF/GFRA-1, IGF-1 and GLP-1 pathways.Metabolic brain disease · 2026Review
- Brain metabolomic profiling reveals ischemia-dominant disruption of metabolic pathways and tissue homeostasis in neonatal hypoxic-ischemic brain injury.Scientific reports · 2026Article
- Neonatal Hypoxic-Ischemic Encephalopathy: From the Limitations of Therapeutic Hypothermia to Precision Intervention.Drug design, development and therapy · 2026Review
- GLP-1 Receptor Agonists in Neurological Disorders: From Mechanisms to Clinical Translation.Drug design, development and therapy · 2026Review
- Semaglutide Mitigates Ischemic Brain Injury by Inhibiting Ferroptosis via Modulation of FoXO1 and DRP1 Pathways.Molecular neurobiology · 2025Article
- Nanoparticle-mediated sodium butyrate delivery for repairing hypoxic-ischemic brain injury in premature infants.Materials today. Bio · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Hypoxic-ischaemic encephalopathy (HIE) arises from diminished blood flow and oxygen to the neonatal brain during labor, leading to infant mortality or severe brain damage, with a global incidence of 1.5 per 1000 live births. Glucagon-like Peptide 1 Receptor (GLP1-R) agonists, used in type 2 diabetes treatment, exhibit neuroprotective effects in various brain injury models, including HIE. In this study, we observed enhanced neurological outcomes in post-natal day 10 mice with surgically induced hypoxic-ischaemic (HI) brain injury after immediate systemic administration of exendin-4 or semaglutide. Short- and long-term assessments revealed improved neuropathology, survival rates, and locomotor function. We explored the mechanisms by which GLP1-R agonists trigger neuroprotection and reduce inflammation following oxygen-glucose deprivation and HI in neonatal mice, highlighting the upregulation of the PI3/AKT signalling pathway and increased cAMP levels. These findings shed light on the neuroprotective and anti-inflammatory effects of GLP1-R agonists in HIE, potentially extending to other neurological conditions, supporting their potential clinical use in treating infants with HIE.
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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 Socratic graph.