ArticleCell death & disease2019
Preso regulates NMDA receptor-mediated excitotoxicity via modulating nitric oxide and calcium responses after traumatic brain injury.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Cognitive effects of intravenous Ketamine in treatment-resistant depression: A systematic review.Psychological medicine · 2026Pooled it
- Parkin protects against traumatic brain injury through regulating mitochondrial quality control.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Molecular mechanisms of excitotoxicity and their relevance to the pathogenesis of neurodegenerative diseases-an update.Acta pharmacologica Sinica · 2025Review
- Animal Models of Traumatic Brain Injury and Their Relevance in Clinical Settings.CNS neuroscience & therapeutics · 2025Review
- Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- The mGluR5-mediated Arc activation protects against experimental traumatic brain injury in rats.CNS neuroscience & therapeutics · 2024Article
- Calcium and Non-Penetrating Traumatic Brain Injury: A Proposal for the Implementation of an Early Therapeutic Treatment for Initial Head Insults.Biomolecules · 2024Review
- LncRNA H19 knockdown promotes neuropathologic and functional recovery via the Nrf2/HO-1 axis after traumatic brain injury.CNS neuroscience & therapeutics · 2024Article
- Preso enhances mGluR1-mediated excitotoxicity by modulating the phosphorylation of mGluR1-Homer1 complex and facilitating an ER stress after traumatic brain injury.Cell death discovery · 2024Article
- Nervous System Response to Neurotrauma: A Narrative Review of Cerebrovascular and Cellular Changes After Neurotrauma.Journal of molecular neuroscience : MN · 2024Review
- Quantitative proteomic and phosphoproteomic analyses of the hippocampus reveal the involvement of NMDAR1 signaling in repetitive mild traumatic brain injury.Neural regeneration research · 2023Article
- The super-enhancer-driven lncRNA LINC00880 acts as a scaffold between CDK1 and PRDX1 to sustain the malignance of lung adenocarcinoma.Cell death & disease · 2023Article
- Single Neuron Modeling Identifies Potassium Channel Modulation as Potential Target for Repetitive Head Impacts.Neuroinformatics · 2023Article
- Pulsed Electromagnetic Fields Protect Against Brain Ischemia by Modulating the Astrocytic Cholinergic Anti-inflammatory Pathway.Cellular and molecular neurobiology · 2023Article
- Anesthesia and analgesia for experimental craniotomy in mice and rats: a systematic scoping review comparing the years 2009 and 2019.Frontiers in neuroscience · 2023Article
- ILBInternational journal of molecular sciences · 2022Article
- Secondary Mechanisms of Neurotrauma: A Closer Look at the Evidence.Diseases (Basel, Switzerland) · 2022Review
- The Development of Novel Drug Treatments for Stroke Patients: A Review.International journal of molecular sciences · 2022Review
- Integrated Proteome and Phosphoproteome Analyses Reveal Early- and Late-Stage Protein Networks of Traumatic Brain Injury.Journal of molecular neuroscience : MN · 2022Article
- Whole Body Vibration Attenuates Brain Damage and Neuroinflammation Following Experimental Traumatic Brain Injury.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) has become a major health concern worldwide, and the poor outcome of TBI increases the need for therapeutic improvement. Secondary injuries following TBI, including excitotoxicity, lead to synaptic dysfunction and provide potential targets for intervention. Postsynaptic scaffold proteins, which are involved in the regulation of excitotoxicity after neuronal injury, play a crucial role in modulating synaptic function. Therefore, exploring the role of postsynaptic scaffold proteins in TBI might uncover new treatments. In this study, we demonstrated that downregulated expression of the postsynaptic scaffold protein Preso protects against neuronal injury after TBI in vitro and in vivo, and these effects are related to the inhibition of N-methyl-D-aspartate receptor (NMDAR) function. Further study showed that Preso facilitates signaling from NMDAR to nitric oxide (NO) and calcium (Ca
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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.