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Astrogliosis
Open accessAbstract
In addition to their many functions in the healthy central nervous system (CNS), astrocytes respond to CNS damage and disease through a process called astrogliosis. For many decades, astrogliosis was sparsely studied and enigmatic. This article examines recent evidence supporting a definition of astrogliosis as a spectrum of heterogeneous potential changes in astrocytes that occur in a context-specific manner as determined by diverse signaling events that vary with the nature and severity of different CNS insults. Astrogliosis is associated with essential beneficial functions, but under specific circumstances can lead to harmful effects. Potential dysfunctions of astrocytes and astrogliosis are being identified that can contribute to, or be primary causes of, CNS disorders, leading to the notion of astrocytopathies. A conceptual framework is presented that allows consideration of normally occurring and dysfunctional astrogliosis and their different roles in CNS disorders.
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“The analysis of individual genes and pathways upregulated in aging astrocytes revealed changes associated with reactive astrocytes, including upregulation of Gfap, Serpina3n, the complement cascade, and cytokines (Sofroniew, 2015; Zamanian et al., 2012).”
From The aging astrocyte transcriptome from multiple regions of the mouse brain. (2018) · cites this paper as Sofroniew, 2015
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“We find that astrocytes in the aging brain exhibit gene expression changes consistent with reactive astrocytes, albeit with changes of a lesser magnitude, showing a mild to moderate level of reactivity (Sofroniew, 2015).”
From The aging astrocyte transcriptome from multiple regions of the mouse brain. (2018) · cites this paper as Sofroniew, 2015
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“Astroglia are interacting with synapses and forming part of the synapse structure [86, 87]”
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“…an injury or a trauma to the CNS, astrocytes undergo a phenomenon called reactivation, which is characterized by profound changes to their structure, gene expression, physiology and function (Barres, 2008; Sofroniew, 2009, 2014; Molofsky et al., 2012; Burda and Sofroniew, 2014; Chung et al., 2015).”
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Radke, J., Schumann, E., Onken, J., Koll, R., Acker, G., Bodnar, B., Senger, C., Tierling, S., Möbs, M., Vajkoczy, P., et al. (2022) · medRxiv · doi:10.1101/2022.02.06.22270509 · Cited by 1
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“…located in the arcuate nucleus of the hypothalamus (ARC) undergo morphological modifications characterized by a hypertrophic phenotype and an increase in glial fibrillary acidic protein (GFAP) immunoreactivity (Horvath et al., 2010, Thaler et al., 2012, Sofroniew, 2014, Escartin et al., 2021).”
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Metadata
- Authors
- Sofroniew, M. V.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Sofroniew, Michael V.
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2014-11-07
- Volume
- 7
- Issue
- 2
- Pages
- a020420
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC4315924
- OpenAlex
- W4239346618
- Cited by
- 695
- References
- 109
- Citations by year
- 2026: 44 · 2025: 53 · 2024: 84 · 2023: 83 · 2022: 101 · 2021: 83 · 2020: 86 · 2019: 61 · 2018: 38 · 2017: 27 · 2016: 21 · 2015: 13 · 2014: 1
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- astrocyte activation, astrocytes, astrocytopathy, central nervous system injury, central nervous system disorders, astrocyte dysfunction
- MeSH terms
- Astrocytes, Cell Communication, Cell Movement, Central Nervous System, Central Nervous System Diseases, Cicatrix, Models, Biological, Mutation, Signal Transduction
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