ArticleNeurochemical research2024
The P38MAPK Pathway Mediates the Destruction of the Blood-Brain Barrier in Anti-NMDAR Encephalitis Mice.
Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Anti-NMDA Receptor Encephalitis Associated with Ovarian Teratoma: A Comprehensive Review.Biomedicines · 2026Review
- Review
- Exercise-Conditioned Endothelial Progenitor Cell-Exosomes Preserve Cerebral Blood Flow and Alleviate Acute Ischemic Brain Injury in Hypertensive Mice.Life (Basel, Switzerland) · 2026Article
- Integrative molecular simulations reveal NeuroAid II mechanisms in ischemic stroke through network pharmacology, molecular dynamics, and pharmacophore modeling.Scientific reports · 2026Article
- Immunopathological mechanisms in autoimmune encephalitis: from pathogenesis to targeted therapies.Frontiers in immunology · 2026Review
- Ligustilide Ameliorates Traumatic Brain Injury in Aged Mice by Attenuating Microglia-Mediated Neuroinflammation.Neurochemical research · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The clinical manifestations of anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis may be closely related to the integrity of the blood-brain barrier (BBB). The P38 mitogen-activated protein kinase (P38MAPK) pathway plays a protective role in neurodegenerative diseases. However, whether the P38MAPK pathway is involved in the underlying mechanism of tight junction (TJ) protein disruption and neuronal damage has not been elucidated. Therefore, in this study, a mouse model of anti-NMDAR encephalitis was established by active immunization with NMDAR NR1
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Registered trials
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