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The complex STATes of astrocyte reactivity: How are they controlled by the JAK-STAT3 pathway?
Open accessAbstract
Astrocytes play multiple important roles in brain physiology. In pathological conditions, they become reactive, which is characterized by morphological changes and upregulation of intermediate filament proteins. Besides these descriptive hallmarks, astrocyte reactivity involves significant transcriptional and functional changes that are far from being fully understood. Most importantly, astrocyte reactivity seems to encompass multiple states, each having a specific influence on surrounding cells and disease progression. These diverse functional states of reactivity must be regulated by subtle signaling networks. Many signaling cascades have been associated with astrocyte reactivity, but among them, the JAK-STAT3 pathway is emerging as a central regulator. In this review, we aim (i) to show that the JAK-STAT3 pathway plays a key role in the control of astrocyte reactivity, (ii) to illustrate that STAT3 is a pleiotropic molecule operating multiple functions in reactive astrocytes, and (iii) to suggest that each specific functional state of reactivity is governed by complex molecular interactions within astrocytes, which converge on STAT3. More research is needed to precisely identify the signaling networks controlling the diverse states of astrocyte reactivity. Only then, we will be able to precisely delineate the therapeutic potential of reactive astrocytes in each neurological disease context.
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“strong evidence implicates a pivotal role of STAT3 in regulating astrogliosis and astrocyte reactivity in AD (Ceyzeriat et al., 2016).”
From Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s Disease (2018) · cites this paper as Ceyzeriat et al., 2016
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Metadata
- Authors
- Ceyzériat, K., Abjean, L., Carrillo-de Sauvage, M.-A., Ben Haim, L., & Escartin, C.
- Affiliations
- Université Paris-Sud (FR)
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2016-08
- Volume
- 330
- Pages
- 205-218
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2400419369
- Cited by
- 185
- References
- 141
- Citations by year
- 2026: 14 · 2025: 19 · 2024: 18 · 2023: 30 · 2022: 22 · 2021: 25 · 2020: 19 · 2019: 16 · 2018: 14 · 2017: 8
- FWCI
- 1.27
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Agence Nationale de la Recherche (ANR-10-JCJC-1402, 2011-BSV4-021-03)
- Centre National de la Recherche Scientifique
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- astrocyte activation, JAK/STAT3 signaling, STAT3, reactive astrocytes, intermediate filament proteins, neurological disorders
- MeSH terms
- Animals, Astrocytes, Humans, Signal Transduction, STAT3 Transcription Factor, Janus Kinases
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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 ›
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