ReviewExpert review of neurotherapeutics2016
Defining the therapeutic time window for suppressing the inflammatory prostaglandin E2 signaling after status epilepticus.
Review in Expert review of neurotherapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 38 citations in OpenAlex.
- Lipoxygenase (LOX) signaling in epilepsy: Pathophysiology and therapeutic prospects.Neurobiology of disease · 2026Review
- Development of highly potent EP2 antagonists as novel anti-inflammatory neuroprotectants.Bioorganic & medicinal chemistry · 2026Article
- Status epilepticus-induced 12/15-lipoxygenase drives neuroinflammation and contributes to neuronal injuries and behavioral comorbidities.Acta pharmacologica Sinica · 2026Article
- Modulating inflammatory prostaglandin E2 signaling to mitigate neurobehavioral comorbidities associated with seizure disorders.Acta pharmaceutica Sinica. B · 2025Review
- The inducible prostaglandin E synthase (mPGES-1) in neuroinflammatory disorders.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Neuroinflammatory mediators in acquired epilepsy: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Transient inhibition of microsomal prostaglandin E synthase-1 after status epilepticus blunts brain inflammation and is neuroprotective.Molecular brain · 2023Article
- Insight into Drug Resistance in Status Epilepticus: Evidence from Animal Models.International journal of molecular sciences · 2023Review
- Prostaglandin E2 in neuroblastoma: Targeting synthesis or signaling?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Neuroprotective Effect of Exogenous Galectin-1 in Status Epilepticus.Molecular neurobiology · 2022Article
- Article
- Effect of taking aspirin before diagnosis on the prognosis of esophageal squamous cell carcinoma and analysis of prognostic factors.The Journal of international medical research · 2022Article
- Inhibition of TRPC3 channels by a novel pyrazole compound confers antiseizure effects.Epilepsia · 2022Article
- Inducible Prostaglandin E Synthase as a Pharmacological Target for Ischemic Stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- EP2 Antagonists (2011-2021): A Decade's Journey from Discovery to Therapeutics.Journal of medicinal chemistry · 2021Review
- Small molecules targeting cyclooxygenase/prostanoid cascade in experimental brain ischemia: Do they translate?Medicinal research reviews · 2021Review
- PGE2 receptors in detrusor muscle: Drugging the undruggable for urgency.Biochemical pharmacology · 2021Review
- Prostaglandin E receptors as targets for ischemic stroke: Novel evidence and molecular mechanisms of efficacy.Pharmacological research · 2021Review
- Neuropathophysiological Mechanisms and Treatment Strategies for Post-traumatic Epilepsy.Frontiers in molecular neuroscience · 2021Review
- COX-2/PGEEpilepsia open · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Neuroinflammation is a common feature in nearly all neurological and some psychiatric disorders. Resembling its extraneural counterpart, neuroinflammation can be both beneficial and detrimental depending on the responding molecules. The overall effect of inflammation on disease progression is highly dependent on the extent of inflammatory mediator production and the duration of inflammatory induction. The time-dependent aspect of inflammatory responses suggests that the therapeutic time window for quelling neuroinflammation might vary with molecular targets and injury types. Therefore, it is important to define the therapeutic time window for anti-inflammatory therapeutics, as contradicting or negative results might arise when different treatment regimens are utilized even in similar animal models. Herein, we discuss a few critical factors that can help define the therapeutic time window and optimize treatment paradigm for suppressing the cyclooxygenase-2/prostaglandin-mediated inflammation after status epilepticus. These determinants should also be relevant to other anti-inflammatory therapeutic strategies for the CNS diseases.
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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.