ReviewCNS neuroscience & therapeutics2022
The role of Na
Review in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 56 citations in OpenAlex.
- Carbamazepine preserves systemic ionic homeostasis and hippocampal Atp1a1 expression following pentylenetetrazol-induced seizures in rats.Neurochemical research · 2026Article
- Central toxic effects of an antitumoral bufadienolide: In silico targets and in vivo findings.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Advances in Strategies to Transport Nanoparticles Across the Blood-Brain Barrier for Drug Delivery into the Brain for the Treatment of Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Nonlinear dynamics of seizure suppression via optogenetic modulation of neuron-astrocyte interaction.Scientific reports · 2026Article
- APOE4 reduces hippocampal expression of phosphoglycerate kinase 1 and sodium potassium pump to enhance seizure susceptibility in mice.Neurobiology of disease · 2026Article
- The accumulation of extracellular KScientific reports · 2025Article
- Ion dynamics underlying the seizure delay effect of low-frequency electrical stimulation.PLoS computational biology · 2025Article
- Collapsing Perisomatic Inhibition Leads to Epileptic Fast-Ripple Oscillations Caused by Pseudosynchronous Firing of CA3 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- CysLTJournal of neurochemistry · 2025Article
- Unveiling the role of Na⁺/K⁺-ATPase pump: neurodegenerative mechanisms and therapeutic horizons.Pharmacological reports : PR · 2025Review
- Development and Characterization of Chitosan Nanoparticles Containing Quercetin-β-Cyclodextrin Inclusion Complex for Improved Solubility, Brain Targeting, and Neuroprotective Potential Against Epilepsy.AAPS PharmSciTech · 2025Article
- Research developments in the neurovascular unit and the blood‑brain barrier (Review).Biomedical reports · 2025Review
- NLRP3 inflammasome-mediated disruption of mitochondrial homeostasis in alveolar macrophages contributes to ozone-induced acute lung inflammatory injury.Acta biochimica et biophysica Sinica · 2025Article
- Sodium butyrate ameliorates mitochondrial oxidative stress and alterations in membrane-bound enzyme activities in pentylenetetrazole-induced kindling rat model.Metabolic brain disease · 2025Article
- Depleting parenchymal border macrophages alleviates cerebral edema and neuroinflammation following status epilepticus.Journal of translational medicine · 2024Article
- Outcomes and relevance of emergency percutaneous coronary angiography and intervention after resuscitated cardiac arrest: a retrospective study.BMC cardiovascular disorders · 2024Article
- Channelopathies in epilepsy: an overview of clinical presentations, pathogenic mechanisms, and therapeutic insights.Journal of neurology · 2024Review
- A novel mutation of DNA2 regulates neuronal cell membrane potential and epileptogenesis.Cell death discovery · 2024Article
- Circadian Rhythms of the Blood-Brain Barrier and Drug Delivery.Circulation research · 2024Review
- Deleting IP6K1 stabilizes neuronal sodium-potassium pumps and suppresses excitability.Molecular brain · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Na+-K+-ATPase, a P-type ATP-powered ion transporter on cell membrane, plays a vital role in cellular excitability. Cellular hyperexcitability, accompanied by hypersynchronous firing, is an important basis for seizures/epilepsy. An increasing number of studies point to a significant contribution of Na+-K+-ATPase to epilepsy, although discordant results exist. In this review, we comprehensively summarize the structure and physiological function of Na+-K+-ATPase in the central nervous system and critically evaluate the role of Na+-K+-ATPase in the epileptic brain. Importantly, we further provide perspectives on some possible research directions and discuss its potential as a therapeutic target for the treatment of epilepsy.
Indexed as
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What OpenQuestion holds
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.