ReviewFrontiers in pharmacology2019
Connexins in Astrocyte Migration.
Review in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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
47 citing papers in PubMed, 73 citations in OpenAlex.
- Macrophages sense and follow physiologically relevant KCell communication and signaling : CCS · 2026Article
- Neuroinflammation-induced downregulation of RAB7 in murine astrocytes disrupts endo-lysosomal homeostasis and induces astrogliosis.Cell communication and signaling : CCS · 2026Article
- Acid sphingomyelinase inhibition restores RPE homeostasis and photoreceptor function in preclinical Stargardt macular degeneration models.bioRxiv : the preprint server for biology · 2026Article
- Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics.Scientific reports · 2026Article
- Multi-omic spatially resolved analysis of the neuroinflammatory response to intracortical microelectrode arrays.Biomaterials · 2026Article
- Mitochondrial fission controls astrocyte morphogenesis and organization in the cortex.The Journal of cell biology · 2025Article
- Expression of CD44 and Its Spliced Variants: Innate and Inducible Roles in Nervous Tissue Cells and Their Environment.International journal of molecular sciences · 2025Review
- Extracellular ATP regulates phagocytic activity, mitochondrial respiration, and cytokine secretion of human astrocytic cells.Purinergic signalling · 2025Article
- Role of astrocytes connexins - pannexins in acute brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Structure and function of neurovascular unit in arterial hypertension.Frontiers in molecular neuroscience · 2025Review
- Glial interactions in the formation and plasticity of the corpus callosum.Frontiers in cellular neuroscience · 2025Review
- Effect ofBiomolecules & biomedicine · 2024Article
- A Pro-Inflammatory Stimulus versus Extensive Passaging of DITNC1 Astrocyte Cultures as Models to Study Astrogliosis.International journal of molecular sciences · 2024Article
- Article
- The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes.Biomedicines · 2024Article
- Short-Term Effects of Gamma Stimulation on Neuroinflammation at the Tissue-Electrode Interface in Motor Cortex.Neuromodulation : journal of the International Neuromodulation Society · 2024Article
- A Brain-Protective Sterol from Soft Coral Inhibits Lipopolysaccharide-Induced Matrix Metalloproteinase-9-Mediated Astrocytic Migration.Biomedicines · 2024Article
- Efficient derivation of functional astrocytes from human induced pluripotent stem cells (hiPSCs).PloS one · 2024Article
- N-Acetylcysteine Treats Spinal Cord Injury by Inhibiting Astrocyte Proliferation.Analytical cellular pathology (Amsterdam) · 2024Article
- Inhibition of astroglial hemichannels ameliorates infrasonic noise induced short-term learning and memory impairment.Behavioral and brain functions : BBF · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes have long been considered the supportive cells of the central nervous system, but during the last decades, they have gained much more attention because of their active participation in the modulation of neuronal function. For example, after brain damage, astrocytes become reactive and undergo characteristic morphological and molecular changes, such as hypertrophy and increase in the expression of glial fibrillary acidic protein (GFAP), in a process known as astrogliosis. After severe damage, astrocytes migrate to the lesion site and proliferate, which leads to the formation of a glial scar. At this scar-forming stage, astrocytes secrete many factors, such as extracellular matrix proteins, cytokines, growth factors and chondroitin sulfate proteoglycans, stop migrating, and the process is irreversible. Although reactive gliosis is a normal physiological response that can protect brain cells from further damage, it also has detrimental effects on neuronal survival, by creating a hostile and non-permissive environment for axonal repair. The transformation of astrocytes from reactive to scar-forming astrocytes highlights migration as a relevant regulator of glial scar formation, and further emphasizes the importance of efficient communication between astrocytes in order to orchestrate cell migration. The coordination between astrocytes occurs mainly through Connexin (Cx) channels, in the form of direct cell-cell contact (gap junctions, GJs) or contact between the extracellular matrix and the astrocytes (hemichannels, HCs). Reactive astrocytes increase the expression levels of several proteins involved in astrocyte migration, such as α
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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.