ArticleCellscience2007
Cellular interplay between neurons and glia: toward a comprehensive mechanism for excitotoxic neuronal loss in neurodegeneration.
Article in Cellscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 39 citations in OpenAlex.
- Oxytocin Anti-Apoptotic Potential Mediates Neuroprotection Against 3-Nitropropionic Acid-Induced Huntington's Disease-Like Pathophysiology in Rats: Involvement of Calpain-2/p25 Cdk5/MEF-2 Signaling Pathway.Neurochemical research · 2025Article
- Sesquiterpene-evoked phytochemical toxicity in PC12 neuronal cells reveals a variable degree of oxidative stress and alpha-tocopherol and glutathione-dependent protection.Current research in toxicology · 2024Article
- Glutamate Chemical Exchange Saturation Transfer (GluCEST) Magnetic Resonance Imaging of Rat Brain With Acute Carbon Monoxide Poisoning.Frontiers in neurology · 2022Article
- 4-(E)-{(p-tolylimino)-methylbenzene-1,2-diol} (TIMBD) suppresses HIV1-gp120 mediated production of IL6 and IL8 but not CCL5.Scientific reports · 2017Article
- HIV Protease Inhibitors Alter Amyloid Precursor Protein Processing via β-Site Amyloid Precursor Protein Cleaving Enzyme-1 Translational Up-Regulation.The American journal of pathology · 2017Article
- Zonisamide-loaded triblock copolymer nanomicelles as a novel drug delivery system for the treatment of acute spinal cord injury.International journal of nanomedicine · 2017Article
- Gene expression profiling predicts pathways and genes associated with Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2016Article
- Down-Regulation of Excitatory Amino Acid Transporters EAAT1 and EAAT2 by the Kinases SPAK and OSR1.The Journal of membrane biology · 2015Article
- System xC- is a mediator of microglial function and its deletion slows symptoms in amyotrophic lateral sclerosis mice.Brain : a journal of neurology · 2015Article
- Nanomedicine strategies for treatment of secondary spinal cord injury.International journal of nanomedicine · 2015Review
- Article
- A truncated fragment of Src protein kinase generated by calpain-mediated cleavage is a mediator of neuronal death in excitotoxicity.The Journal of biological chemistry · 2013Article
- Review
- Activating transcription factor 4, a mediator of the integrated stress response, is increased in the dorsal root ganglia following painful facet joint distraction.Neuroscience · 2011Article
- Parallel high throughput neuronal toxicity assays demonstrate uncoupling between loss of mitochondrial membrane potential and neuronal damage in a model of HIV-induced neurodegeneration.Neuroscience research · 2011Article
- Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis.Surgical neurology international · 2011Article
- Characterisation of genome-wide association epistasis signals for serum uric acid in human population isolates.PloS one · 2011Article
- Apolipoprotein E4 domain interaction induces endoplasmic reticulum stress and impairs astrocyte function.The Journal of biological chemistry · 2009Article
- Painful facet joint injury induces neuronal stress activation in the DRG: implications for cellular mechanisms of pain.Neuroscience letters · 2008Article
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 1 institution in 1 country.
Funding
Abstract
Astrocytes perform vital maintenance, functional enhancement, and protective roles for their associated neurons; however these same mechanisms may become deleterious for neurons under some conditions. In this review, we highlight two normally protective pathways, the endoplasmic reticulum (ER) stress response and an endogenous antioxidant response, which may become neurotoxic when activated in astrocytes during the inflammation associated with neurodegeneration. Stimulation of these multifaceted pathways affects a panoply of cellular processes. Of particular importance is the effect these pathways have on the homeostasis of the excitatory amino acid neurotransmitter, glutamate. The endogenous antioxidant response increases extracellular glutamate in the pursuit of making the cellular antioxidant, glutathione, by increasing expression of the xCT subunit of the cystine/glutamate antiporter. Meanwhile, inflammatory mediators such as TNFα reduce levels of membrane-bound glutamate scavenging proteins such as the excitatory amino acid transporters. Together, these cellular activities may result in a net increase in extracellular glutamate that could alter neuronal function and lead to excitotoxicity. Here we discuss the role of N-methyl-D-aspartate receptors, which, when excessively stimulated by glutamate, can cause neuronal dysfunction and loss via activation of calpains. While there are other pathways acting in concert or parallel to those we describe here, this review explores a rationale to explain how two protective mechanisms may result in neuronal loss during neurodegeneration.
Identifiers
19122795PMC2613343W25703051What 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.