ArticleCells2019
NLRX1 Enhances Glutamate Uptake and Inhibits Glutamate Release by Astrocytes.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- The adhesion GPCR ADGRV1 controls glutamate homeostasis in hippocampal astrocytes supporting neurons.Acta neuropathologica communications · 2026Article
- The Protective Role of Aquaporin 4 (AQP4) in Temporal Lobe Epilepsy: Yes or No?Journal of molecular neuroscience : MN · 2026Review
- Astrocytes in maintaining neuronal health and brain function: interplay of aging, diet, and environment.Metabolic brain disease · 2025Review
- Altered metabolic function induced by Aβ-oligomers and PSEN1 mutations in iPSC-derived astrocytes.Journal of neurochemistry · 2025Article
- Progress of Astrocyte-Neuron Crosstalk in Central Nervous System Diseases.Neurochemical research · 2024Review
- Citrullinated isomer of myelin basic protein can induce inflammatory responses in astrocytes.IBRO neuroscience reports · 2024Article
- NLRX1 Inhibits LPS-Induced Microglial Death via Inducing p62-Dependent HO-1 Expression, Inhibiting MLKL and Activating PARP-1.Antioxidants (Basel, Switzerland) · 2024Article
- The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes.Biomedicines · 2024Article
- Salidroside ameliorates cerebral ischemic injury and regulates the glutamate metabolism pathway in astrocytes.Frontiers in pharmacology · 2024Article
- Review
- Astroglial Connexin 43-Mediated Gap Junctions and Hemichannels: Potential Antidepressant Mechanisms and the Link to Neuroinflammation.Cellular and molecular neurobiology · 2023Review
- An in vitro study on the stimulatory effects of extracellular glutamate on astrocytes.Molecular biology reports · 2023Article
- Circular RNA Tmcc1 improves astrocytic glutamate metabolism and spatial memory via NF-κB and CREB signaling in a bile duct ligation mouse model: transcriptional and cellular analyses.Journal of neuroinflammation · 2023Article
- The regulation of self-tolerance and the role of inflammasome molecules.Frontiers in immunology · 2023Review
- Novel Antidepressant Mechanism of Ginsenoside Rg1 in Regulating the Dysfunction of the Glutamatergic System in Astrocytes.International journal of molecular sciences · 2022Article
- Excitatory Synaptic Transmission in Ischemic Stroke: A New Outlet for Classical Neuroprotective Strategies.International journal of molecular sciences · 2022Review
- Hypercapnia Modulates the Activity of Adenosine A1 Receptors and mitoKNeuromolecular medicine · 2022Article
- Astrocytic Glutamatergic Transmission and Its Implications in Neurodegenerative Disorders.Cells · 2022Review
- Effects of early noise exposure on hippocampal-dependent behaviors during adolescence in male rats: influence of different housing conditions.Animal cognition · 2022Article
- Metabolic regulators of enigmatic inflammasomes in autoimmune diseases and crosstalk with innate immune receptors.Immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uptake of glutamate from the extracellular space and glutamate release to neurons are two major processes conducted by astrocytes in the central nervous system (CNS) that protect against glutamate excitotoxicity and strengthen neuronal firing, respectively. During inflammatory conditions in the CNS, astrocytes may lose one or both of these functions, resulting in accumulation of the extracellular glutamate, which eventually leads to excitotoxic neuronal death, which in turn worsens the CNS inflammation. NLRX1 is an innate immune NOD-like receptor that inhibits the major inflammatory pathways. It is localized in the mitochondria and was shown to inhibit cell death, enhance ATP production, and dampen oxidative stress. In the current work, using primary murine astrocyte cultures from WT and
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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.