ArticlePathophysiology : the official journal of the International Society for Pathophysiology2007
Disruption of ionic and cell volume homeostasis in cerebral ischemia: The perfect storm.
Article in Pathophysiology : the official journal of the International Society for Pathophysiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 96 citations in OpenAlex.
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- An approach based on linear programming to build experimentally driven pump-leak models.Biophysical journal · 2026Article
- Assessing low-dose lithium salts for Varroa mite (Varroa destructor) management in honeybees (Apis mellifera): field efficacy and health implications.Experimental & applied acarology · 2025Article
- Review
- From inflammatory signaling to neuronal damage: Exploring NLR inflammasomes in ageing neurological disorders.Heliyon · 2024Review
- Advanced Nano-Drug Delivery Systems in the Treatment of Ischemic Stroke.Molecules (Basel, Switzerland) · 2024Review
- Astrocyte Regulation of Neuronal Function and Survival in Stroke Pathophysiology.Advances in neurobiology · 2024Review
- The NLRP3 inflammasome and gut dysbiosis as a putative link between HIV-1 infection and ischemic stroke.Trends in neurosciences · 2023Review
- Abnormal Spontaneous Discharges of Primary Sensory Neurons and Pain Behavior in a Rat Model of Vascular Dementia.International journal of molecular sciences · 2023Article
- Conditional deletion of LRRC8A in the brain reduces stroke damage independently of swelling-activated glutamate release.iScience · 2023Article
- Directly targeting ASC by lonidamine alleviates inflammasome-driven diseases.Journal of neuroinflammation · 2022Article
- Advances of nano drug delivery system for the theranostics of ischemic stroke.Journal of nanobiotechnology · 2022Review
- The role of inflammasomes in vascular cognitive impairment.Molecular neurodegeneration · 2022Review
- Late adolescence mortality in mice with brain-specific deletion of the volume-regulated anion channel subunit LRRC8A.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion.Biomedicines · 2021Review
- Review
- Rapid Neuronal Ultrastructure Disruption and Recovery during Spreading Depolarization-Induced Cytotoxic Edema.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 1: Roles of VSOR/VRAC in Cell Volume Regulation, Release of Double-Edged Signals and Apoptotic/Necrotic Cell Death.Frontiers in cell and developmental biology · 2020Review
- Inhibition of NLRP3 Inflammasome: A Prospective Target for the Treatment of Ischemic Stroke.Frontiers in cellular neuroscience · 2020Review
- Metabolic constraints of swelling-activated glutamate release in astrocytes and their implication for ischemic tissue damage.Journal of neurochemistry · 2019Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The mechanisms of brain tissue damage in stroke are strongly linked to the phenomenon of excitotoxicity, which is defined as damage or death of neural cells due to excessive activation of receptors for the excitatory neurotransmitters glutamate and aspartate. Under physiological conditions, ionotropic glutamate receptors mediate the processes of excitatory neurotransmission and synaptic plasticity. In ischemia, sustained pathological release of glutamate from neurons and glial cells causes prolonged activation of these receptors, resulting in massive depolarization and cytoplasmic Ca(2+) overload. High cytoplasmic levels of Ca(2+) activate many degradative processes that, depending on the metabolic status, cause immediate or delayed death of neural cells. This traditional view has been expanded by a number of observations that implicate Cl(-) channels and several types of non-channel transporter proteins, such as the Na(+),K(+),2Cl(-) cotransporter, Na(+)/H(+) exchanger, and Na(+)/Ca(2+) exchanger, in the development of glutamate toxicity. Some of these ion transporters increase tissue damage by promoting pathological cell swelling and necrotic cell death, while others contribute to a long-term accumulation of cytoplasmic Ca(2+). This brief review is aimed at illustrating how the dysregulation of various ion transport processes combine in a 'perfect storm' that disrupts neural ionic homeostasis and culminates in the irreversible damage and death of neural cells. The clinical relevance of individual transporters as targets for therapeutic intervention in stroke is also briefly discussed.
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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.