ArticlePharmaceutics2022
Activation of NLRP3 Is Required for a Functional and Beneficial Microglia Response after Brain Trauma.
Article in Pharmaceutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- The Role of Neuroinflammation in Shaping Neuroplasticity and Recovery Outcomes Following Traumatic Brain Injury: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- New Strategies for Treating Depression with Chinese Medicine: Focusing on NLRP3-Mediated Mechanisms.Chinese journal of integrative medicine · 2026Review
- Autosomal Dominant Polycystic Kidney Disease-Related Multifocal Renal Cell Carcinoma: A Narrative Iconographic Review.International journal of molecular sciences · 2025Review
- Protective Effects of Mdivi-1 on Cognition Disturbance Following Sepsis in Mice via Alleviating Microglia Activation and Polarization.CNS neuroscience & therapeutics · 2025Article
- Targeting inflammasome pathway towards therapeutics of neurodegenerative diseases.Organelle (Tucson, Ariz.) · 2025Article
- Article
- Inflammasomes in neurological disorders - mechanisms and therapeutic potential.Nature reviews. Neurology · 2024Review
- Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome.Neurochemical research · 2024Article
- The role of mtDAMPs in the trauma-induced systemic inflammatory response syndrome.Frontiers in immunology · 2023Review
- NLRP-3 Inflammasome: A Key Target, but Mostly Overlooked following SARS-CoV-2 Infection.Vaccines · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Despite the numerous research studies on traumatic brain injury (TBI), many physiopathologic mechanisms remain unknown. TBI is a complex process, in which neuroinflammation and glial cells play an important role in exerting a functional immune and damage-repair response. The activation of the NLRP3 inflammasome is one of the first steps to initiate neuroinflammation and so its regulation is essential. Using a closed-head injury model and a pharmacological (MCC950; 3 mg/kg, pre- and post-injury) and genetical approach (NLRP3 knockout (KO) mice), we defined the transcriptional and behavioral profiles 24 h after TBI. Wild-type (WT) mice showed a strong pro-inflammatory response, with increased expression of inflammasome components, microglia and astrocytes markers, and cytokines. There was no difference in the IL1β production between WT and KO, nor compensatory mechanisms of other inflammasomes. However, some microglia and astrocyte markers were overexpressed in KO mice, resulting in an exacerbated cytokine expression. Pretreatment with MCC950 replicated the behavioral and blood-brain barrier results observed in KO mice and its administration 1 h after the lesion improved the damage. These findings highlight the importance of NLRP3 time-dependent activation and its role in the fine regulation of glial response.
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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.