ReviewTranslational stroke research2014
Ionic regulation of cell volume changes and cell death after ischemic stroke.
Review in Translational stroke research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 117 citations in OpenAlex.
- Shrinking of Extracellular Space During Metabolic Stress Accelerates Amyloid-β Aggregation.Biomolecules · 2026Article
- Targeting PKC/NF-κB/NLRP3-driven NcRNA neuroinflammatory crosstalk by condensed tannins in global cerebral ischemia.Inflammopharmacology · 2026Review
- NMDA receptor mediated tonic excitatory currents are elicited by EAAT inhibition on human neocortical pyramidal neurons.Frontiers in synaptic neuroscience · 2026Article
- Gamma-Benzylidene Digoxin Derivative Attenuates Neurotoxicity Response in a Murine Stroke Model.Translational stroke research · 2025Article
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- Revealing membrane integrity and cell size from diffusion kurtosis time dependence.Magnetic resonance in medicine · 2025Article
- Unleashing the potential: 40 Hz multisensory stimulation therapy for cognitive impairment.Journal of central nervous system disease · 2025Review
- Glymphatic system function in patients with ischemic stroke evaluated by the DTI-ALPS method: a comprehensive review.Frontiers in neurology · 2025Review
- Elucidating multifaceted targets of Marein in cerebral ischemia-reperfusion injury.Frontiers in chemistry · 2025Article
- Molecular Mechanism of MLC 901 in Acute Ischemic Stroke: A Review.Stroke research and treatment · 2025Review
- Dual Role of TRPV1 Channels in Cerebral Stroke: An Exploration from a Mechanistic and Therapeutic Perspective.Molecular neurobiology · 2024Review
- Ion Channel Dysregulation Following Intracerebral Hemorrhage.Neuroscience bulletin · 2024Review
- Innovations in Breaking Barriers: Liposomes as Near-Perfect Drug Carriers in Ischemic Stroke Therapy.International journal of nanomedicine · 2024Review
- ALS-like pathology diminishes swelling of spinal astrocytes in the SOD1 animal model.Frontiers in cellular neuroscience · 2024Article
- The role ofJournal of pharmaceutical analysis · 2023Review
- Extrasynaptic NMDA receptors in acute and chronic excitotoxicity: implications for preventive treatments of ischemic stroke and late-onset Alzheimer's disease.Molecular neurodegeneration · 2023Review
- Transient receptor potential ion channels and cerebral stroke.Brain and behavior · 2023Review
- Pathogenesis of sporadic Alzheimer's disease by deficiency of NMDA receptor subunit GluN3A.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury.Frontiers in cellular neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Stroke is a leading cause of human death and disability in the USA and around the world. Shortly after the cerebral ischemia, cell swelling is the earliest morphological change in injured neuronal, glial, and endothelial cells. Cytotoxic swelling directly results from increased Na(+) (with H2O) and Ca(2+) influx into cells via ionic mechanisms evoked by membrane depolarization and a number of harmful factors such as glutamate accumulation and the production of oxygen reactive species. During the sub-acute and chronic phases after ischemia, injured cells may show a phenotype of cell shrinkage due to complex processes involving membrane receptors/channels and programmed cell death signals. This review will introduce some progress in the understanding of the regulation of pathological cell volume changes and the involved receptors and channels, including NMDA and AMPA receptors, acid-sensing ion channels, hemichannels, transient receptor potential channels, and KCNQ channels. Moreover, accumulating evidence supports a key role of energy deficiency and dysfunction of Na(+)/K(+)-ATPase in ischemia-induced cell volume changes and cell death. Specifically, the Na(+) pump failure is a prerequisite for disruption of ionic homeostasis including a pro-apoptotic disruption of the K(+) homeostasis. Finally, we will introduce the concept of hybrid cell death as a result of the Na(+) pump failure in cultured cells and the ischemic brain. The goal of this review is to outline recent understanding of the ionic mechanism of ischemic cytotoxicity and suggest innovative ideas for future translational research.
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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.