ArticleMolecular neurobiology2017
Inhibition of the Receptor for Advanced Glycation End-Products (RAGE) Attenuates Neuroinflammation While Sensitizing Cortical Neurons Towards Death in Experimental Subarachnoid Hemorrhage.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- RAGE-Mediated Signalling in Gynaecological Disorders: Review of Molecular Mechanisms and Therapeutic Perspectives.Expert reviews in molecular medicine · 2026Review
- Article
- Recombinant soluble form of receptor for advanced glycation end products ameliorates microcirculation impairment and neuroinflammation after subarachnoid hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- RAGE Inhibitors as Alternatives to Dexamethasone for Managing Cerebral Edema Following Brain Tumor Surgery.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration.Nutrients · 2022Review
- High-mobility Group Box 1 Contributes to Hypoxic-Ischemic Brain Damage by Facilitating Imbalance of Microglial Polarization through RAGE-PI3K/Akt Pathway in Neonatal Rats.International journal of medical sciences · 2022Article
- Pathophysiology of RAGE in inflammatory diseases.Frontiers in immunology · 2022Review
- Berberine Ameliorates Subarachnoid Hemorrhage InjuryFrontiers in pharmacology · 2020Article
- Exogenous brain-derived neurotrophic factor attenuates neuronal apoptosis and neurological deficits after subarachnoid hemorrhage in rats.Experimental and therapeutic medicine · 2019Article
- The Receptor for Advanced Glycation End Products (RAGE) and DIAPH1: Implications for vascular and neuroinflammatory dysfunction in disorders of the central nervous system.Neurochemistry international · 2019Review
- Relation of postoperative serum S100A12 levels to delirium and cognitive dysfunction occurring after hip fracture surgery in elderly patients.Brain and behavior · 2019Observational
- The rise of soluble platelet-derived growth factor receptor β in CSF early after subarachnoid hemorrhage correlates with cerebral vasospasm.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2018Article
- Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-Behavioural neurology · 2018Article
- Autophagy after Subarachnoid Hemorrhage: Can Cell Death be Good?Current neuropharmacology · 2018Review
- Inhibition of myeloid differentiation primary response protein 88 provides neuroprotection in early brain injury following experimental subarachnoid hemorrhage.Scientific reports · 2017Article
- Delayed Cerebral Ischemia after Subarachnoid Hemorrhage: Beyond Vasospasm and Towards a Multifactorial Pathophysiology.Current atherosclerosis reports · 2017Review
- Heparin and Heparin-Derivatives in Post-Subarachnoid Hemorrhage Brain Injury: A Multimodal Therapy for a Multimodal Disease.Molecules (Basel, Switzerland) · 2017Review
- Roles of Pannexin-1 Channels in Inflammatory Response through the TLRs/NF-Kappa B Signaling Pathway Following Experimental Subarachnoid Hemorrhage in Rats.Frontiers in molecular neuroscience · 2017Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subarachnoid hemorrhage (SAH) is a threatening and devastating neurological insult with high mortality and morbidity rates. Despite considerable efforts, the underlying pathophysiological mechanisms are still poorly understood. The receptor for advanced glycation end products (RAGE) is a multiligand receptor that has been implicated in various pathological conditions. We previously showed that RAGE was upregulated and may be involved in pathophysiology of SAH. In the current study, we investigated its potential role in SAH. We found that the upregulation of RAGE after SAH was NF-κB-dependent positive feedback regulation. Further, pharmacological inhibition of RAGE attenuated neuroinflammation, indicating a possible contributive role of RAGE in inflammation-associated brain injury after SAH. Conversely, however, inhibition of RAGE sensitized neurons, exacerbating cell death, which correlated with augmented apoptosis and diminished autophagy, suggesting that activation of RAGE may protect against SAH-induced neuronal injury. Furthermore, we demonstrate that inhibition of RAGE significantly reduced brain edema and improved neurological function at day 1 but not at day 3 post-SAH. Taken together, these results suggest that RAGE exerts dual role after SAH. Our findings also suggest caution should be exercised in setting RAGE-targeted treatment for SAH.
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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.