ReviewNeurochemical research2000
Phospholipases A2 in ischemic and toxic brain injury.
Review in Neurochemical research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Metabolomic Investigation of β-Thalassemia in Chorionic Villi Samples.Journal of clinical medicine · 2019Article
- Protective effects of celecoxib on ischemia reperfusion-induced acute kidney injury: comparing between male and female rats.Iranian journal of basic medical sciences · 2019Article
- Article
- Therapies targeting lipid peroxidation in traumatic brain injury.Brain research · 2016Review
- Metabolomics Approach Reveals Integrated Metabolic Network Associated with Serotonin Deficiency.Scientific reports · 2015Article
- sPLA2 IB induces human podocyte apoptosis via the M-type phospholipase A2 receptor.Scientific reports · 2014Article
- Cytosolic phospholipase A2 protein as a novel therapeutic target for spinal cord injury.Annals of neurology · 2014Article
- Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.PloS one · 2013Article
- Significance of brain tissue oxygenation and the arachidonic acid cascade in stroke.Antioxidants & redox signaling · 2011Review
- Study on the relationship of cPLA2, CK-MB, and membrane phospholipid content in acute myocardial infarction.Heart and vessels · 2011Article
- Phospholipase A2 and its molecular mechanism after spinal cord injury.Molecular neurobiology · 2010Review
- Low molecular weight phospholipases A2 in mammalian brain and neural cells: roles in functions and dysfunctions.Molecular neurobiology · 2010Review
- Nanomolar vitamin E alpha-tocotrienol inhibits glutamate-induced activation of phospholipase A2 and causes neuroprotection.Journal of neurochemistry · 2010Article
- Metabotropic glutamate receptors as targets for multipotential treatment of neurological disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
- The cytotoxic effect of bromoenol lactone, a calcium-independent phospholipase A2 inhibitor, on rat cortical neurons in culture.Cellular and molecular neurobiology · 2008Article
- Cytosolic phospholipase A2 alpha inhibition prevents neuronal NMDA receptor-stimulated arachidonic acid mobilization and prostaglandin production but not subsequent cell death.Journal of neurochemistry · 2008Article
- Role of secretory phospholipase a(2) in CNS inflammation: implications in traumatic spinal cord injury.CNS & neurological disorders drug targets · 2008Review
- Arachidonic acid metabolism in brain physiology and pathology: lessons from genetically altered mouse models.Journal of neurochemistry · 2007Review
- Radical scavenger can scavenge lipid allyl radicals complexed with lipoxygenase at lower oxygen content.The Biochemical journal · 2006Article
- Cytoprotection by glycine against ATP-depletion-induced injury is mediated by glycine receptor in renal cells.The Biochemical journal · 2005Article
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.
Funding
Abstract
Phospholipases A2 (PLA2s) regulate hydrolysis of fatty acids, including arachidonic acid, from the sn-2 position of phospholipid membranes. PLA2 activity has been implicated in neurotoxicity and neurodegenerative processes secondary to ischemia and reperfusion and other oxidative stresses. The PLA2s constitute a superfamily whose members have diverse functions and patterns of expression. A large number of PLA2s have been identified within the central nervous systems of rodents and humans. We postulated that group IV large molecular weight, cytosolic phospholipase A2 (cPLA2) has a unique role in neurotoxicity associated with ischemic or toxin stress. We created mice deficient in cPLA2 and tested this hypothesis in two injury models, ischemia/reperfusion and MPTP neurotoxicity. In each model cPLA2 deficient mice are protected against neuronal injury when compared to their wild type littermate controls. These experiments support the hypothesis that cPLA2 is an important mediator of ischemic and oxidative injuries in the brain.
Indexed as
Identifiers
10905638What 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.