Multiple Roles for Astrocytes as Effectors of Cytokines and Inflammatory Mediators
Abstract
Astrocytes are increasingly recognized as exerting complex functions essential for normal neural activity in the healthy central nervous system (CNS). Because astrocytes also respond to all forms of CNS injury or disease, there is growing interest in how reactive astrogliosis might alter astrocyte functions and thereby affect neural functions. Reactive astrogliosis is heterogeneous and regulated in a context specific manner by different molecular signals. Prominent among astrocyte signaling mechanisms is the ability to respond to, as well as to produce, many different cytokines and inflammatory mediators. These signaling mechanisms enable astrocytes to interact with diverse cell types in ways that may contribute to crosstalk between immune/inflammatory and neural systems. Consistent with this notion is the increasing evidence that cytokines and inflammatory mediators modulate astrocyte signaling not only to influence immune and inflammatory activities in the CNS, but also to influence synaptic and neural functions in ways that may affect complex behaviors such as sickness behavior, pain, appetite, sleep, and mood.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the AD and PD brain, both astrocytes and microglia acquire reactive, inflammatory phenotypes and can effectively phagocytose aggregated proteins and cell debris, as well as secrete various cytokines and inflammatory mediators.
“In the AD and PD brain, both astrocytes and microglia acquire reactive, inflammatory phenotypes and can effectively phagocytose aggregated proteins and cell debris, as well as secrete various cytokines and inflammatory mediators [8–13].”
From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [9]
Microglia and astrocytes are responsible for many inflammatory processes in affected brains, including phagocytosis of αSYN and Aβ aggregates, secretion of inflammatory mediators, and stimulation of the innate immune system.
“Microglia and astrocytes are known to be responsible for many inflammatory processes in affected brains, including phagocytosis of αSYN and Aβ aggregates, secretion of inflammatory mediators, and stimulation of the innate immune system [8–12].”
From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [9]
No citation lists for this paper
No citation lists for this paper yet — checked again daily.
References 96 · Cited by 333
- Authors
- Sofroniew, M. V.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Sofroniew, Michael V.
- Venue
- The Neuroscientist
- Publisher
- SAGE Publications
- Published
- 2013-10-08
- Volume
- 20
- Issue
- 2
- Pages
- 160-172
- ISSN
- 1073-8584 (ISSN-L)
- 1089-4098
- OpenAlex
- W2095369231
- Cited by
- 333
- References
- 96
- Citations by year
- 2026: 13 · 2025: 13 · 2024: 23 · 2023: 25 · 2022: 32 · 2021: 31 · 2020: 40 · 2019: 37 · 2018: 34 · 2017: 26 · 2016: 18 · 2015: 27 · 2014: 12 · 2013: 1
- FWCI
- 10.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Neuroscientist (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS057624, R01NS057624)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- astrocytes, reactive astrogliosis, cytokines, inflammatory mediators, astrocyte signaling, neuroinflammation, synaptic function, sickness behavior, pain, sleep, mood
- MeSH terms
- Animals, Astrocytes, Humans, Neuroimmunomodulation, Cytokines
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review