ArticleJournal of neuroinflammation2022
Flufenamic acid improves survival and neurologic outcome after successful cardiopulmonary resuscitation in mice.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Genetic inactivation of TRPM4 does not alter the temperature-dependent movement of mouse microglia.The journal of physiological sciences : JPS · 2026Article
- Bindarit attenuates brain injury and neuroinflammation in status epilepticus by disrupting C3/C3aR signaling and modulating microglia-astrocyte interactions.Cell communication and signaling : CCS · 2026Article
- Sphingosine-1-Phosphate Receptor 3 Mediated Neuroinflammation is Critically Involved in the Development of Brain Injury Following Cardiac Arrest in Mice.Neurochemical research · 2026Article
- Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy.Cellular and molecular neurobiology · 2026Article
- Inflammation-responsive biomimetic hybrid nanovesicles reverse stem cell senescence by up-regulating SIRT1 to treat periodontitis.Journal of nanobiotechnology · 2026Article
- SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Cardiac arrest triggers IL-17-mediated neuroinflammation and astrocyte polarization: insights into pathogenesis and intervention.Journal of neuroinflammation · 2025Article
- Potentiating microglial efferocytosis by MFG-E8 improves survival and neurological outcome after successful cardiopulmonary resuscitation in mice.Brain pathology (Zurich, Switzerland) · 2025Article
- Gut-derived macrophages link intestinal damage to brain injury after cardiac arrest through TREM1 signaling.Cellular & molecular immunology · 2025Article
- Translational approach to assess brain injury after cardiac arrest in preclinical models: a narrative review.Intensive care medicine experimental · 2025Review
- GYY4137 ameliorates blood brain barrier damage by inhibiting autophagy mediated occludin degradation in cardiac arrest and resuscitation.Scientific reports · 2025Article
- Unlocking the potential of cardiac TRP channels using knockout mice models.Frontiers in physiology · 2025Article
- Neuroprotective Approaches for Brain Injury After Cardiac Arrest: Current Trends and Prospective Avenues.Journal of stroke · 2024Review
- Antiseizure properties of fenamate NSAIDs determined in mature human stem-cell derived neuroglial circuits.Frontiers in pharmacology · 2024Article
- The TRPM4 channel inhibitor 9-phenanthrol alleviates cerebral edema after traumatic brain injury in rats.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBrain injury is the main cause of high mortality and disability after successful cardiopulmonary resuscitation (CPR) from sudden cardiac arrest (CA). The transient receptor potential M4 (TRPM4) channel is a novel target for ameliorating blood-brain barrier (BBB) disruption and neuroinflammation. Herein, we tested whether flufenamic acid (FFA), which is reported to block TRPM4 with high potency, could confer neuroprotection against brain injury secondary to CA/CPR and whether its action was exerted by blocking the TRPM4 channel.
methodsWild-type (WT) and Trpm4 knockout (Trpm4
resultsIn WT mice subjected to CA/CPR, FFA was effective in improving survival and neurologic outcome, reducing neuropathological injuries, attenuating brain edema, lessening the leakage of IgG and Evans blue dye, restoring tight junction protein expression and promoting microglia/macrophages from the pro-inflammatory subtype toward the anti-inflammatory subtype. In comparison to WT mice, Trpm4
conclusionsFFA mitigates BBB breach and modifies the functional status of microglia/macrophages, thereby improving survival and neurologic deficits following CA/CPR. The neuroprotective effects occur at least partially by interfering with the TRPM4 channel in the neurovascular unit. These results indicate the significant clinical potential of FFA to improve the prognosis for CA victims who are successfully resuscitated.
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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.