Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (470 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from star cells) are irregularly shaped with many long processes, including those with end feet which form the glial (limiting) membrane and directly and indirectly contribute to the blood-brain barrier. They regulate the extracellular ionic and chemical environment, and reactive astrocytes (along with microglia) respond to injury.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Astrocyte; Astroglia Cells; Astroglia Cell; Cell, Astroglia; Astroglial Cells; Astroglial Cell; Cell, Astroglial; Astroglia.
Where it fits in the MeSH classification
- Broader topics
- Neuroglia
- See also
- Blood-Brain Barrier
Related concepts
Research landscape
PubMed indexes 44,042 records tagged with the MeSH heading “Astrocytes” (counts retrieved 2026-10-29). 10,099 of them (22.9%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 13,968 records.
Reviews account for 4,603 records (10.5%) and meta-analyses for 29. Randomized controlled trials number 14 (0.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 9,725 |
| 2000-2009 | 10,250 |
| 2010-2019 | 13,968 |
| 2020 onward | 10,099 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 4,603 | 10.5% |
| Meta-analyses | 29 | 0.1% |
| Randomized controlled trials | 14 | 0.0% |
Method: PubMed query "Astrocytes"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Astrocytes enable amygdala neural representations supporting memory | 2026 | Research article Design not recorded in structured metadata | 12 | cc by PMID 41673152 · DOI · PMC13061616 |
| NF-κB activation in astrocytes impairs wound healing after traumatic brain injury in male mice | 2026 | Research article Design not recorded in structured metadata | 8 | cc by PMID 41792174 · DOI · PMC12976058 |
| Astrocyte States in Brain Aging and Neurodegeneration: At the Crossroads of Senescence and Reactivity | 2026 | Review article Design not recorded in structured metadata | 7 | cc by PMID 41803335 · DOI · PMC12971753 |
Astrocytes enable amygdala neural representations supporting memory [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Brain systems mediating responses to previously encountered threats provide critical survival functions.
- Closing excerpt
- Our findings reveal a key role for astrocytes in the generation and adaptation of fear-state-related neural representations, revising neurocentric models of critical amygdala-mediated adaptive functions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (126 words)
Brain systems mediating responses to previously encountered threats provide critical survival functions. Fear memory and extinction are underpinned by neural representations in the basolateral amygdala (BLA)1-7, but the contribution of non-neuronal cells, including astrocytes, to these processes remains unresolved. Here, using in vivo calcium (Ca2+) imaging and causal astrocyte manipulations, we find that BLA astrocytes dynamically track fear state and support fear memory retrieval and extinction. By combining astrocyte manipulations with in vivo BLA neuronal Ca2+ imaging and electrophysiological recordings, we show that astrocyte Ca2+ signalling enables neuronal encoding of fear memory retrieval and extinction, and readout through a BLA-prefrontal circuit. Our findings reveal a key role for astrocytes in the generation and adaptation of fear-state-related neural representations, revising neurocentric models of critical amygdala-mediated adaptive functions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41673152 · DOI · PMC13061616
NF-κB activation in astrocytes impairs wound healing after traumatic brain injury in male mice [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Traumatic brain injury (TBI) is a complex condition in which multiple pathophysiological mechanisms influence the course of the disease.
- Closing excerpt
- These findings enhance our understanding on the NF-κB-mediated post-traumatic pathophysiology and provide information on future targeted therapies to improve TBI outcome.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (146 words)
Traumatic brain injury (TBI) is a complex condition in which multiple pathophysiological mechanisms influence the course of the disease. After the initial mechanical impact, neuroinflammatory reactions of glial cells along with infiltrating peripheral immune cells determine the overall clinical outcome. However, these secondary processes and their molecular determinants promoting either beneficial or detrimental consequences are not well-defined. Here, we show that TBI-mediated NF-κB activation in astrocytes impairs their homeostatic functions, amplifies the post-traumatic neuroimmune response and disturbs the multicellular CNS scar development in a male mouse model of TBI. Our results further demonstrate a specific deficit in the formation of the glial limitans border and establish that paracrine signaling pathways induced by NF-κB-activated astrocytes can prevent a beneficial restoration of the CNS integrity after TBI. These findings enhance our understanding on the NF-κB-mediated post-traumatic pathophysiology and provide information on future targeted therapies to improve TBI outcome.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41792174 · DOI · PMC12976058
Astrocyte States in Brain Aging and Neurodegeneration: At the Crossroads of Senescence and Reactivity [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Brain aging involves progressive disruption of tissue homeostasis and susceptibility to neurodegenerative disorders.
- Closing excerpt
- We argue that resolving these issues is essential for advancing therapeutic strategies that specifically target defined astrocyte phenotypes, rather than nonspecifically suppressing astrocyte activity, in aging and neurodegenerative diseases.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
Brain aging involves progressive disruption of tissue homeostasis and susceptibility to neurodegenerative disorders. Within this context, astrocytes are key determinants of region-specific physiology, given their roles in metabolic support, synapse regulation, proteostasis, neuroinflammation, and blood-brain barrier maintenance. Aging is accompanied by broad transcriptional and functional remodeling in astrocytes, leading to the emergence of distinct cellular states that cannot be defined by classical morphological criteria alone. This review discusses how aging modifies astrocyte identities toward reactive and senescence-like states. We summarize core features of astrocyte senescence, including altered secretory signaling, impaired neuronal support, and changes in mitochondrial and proteostatic pathways, while integrating recent single-cell and regionally transcriptomic studies that delineate multiple reactive states associated with aging and pathological contexts. We further address evidence that reactivity and senescence are not mutually exclusive endpoints, but may coexist, arise sequentially, or partially overlap depending on timing, brain region, biological sex, and pathological insults. Finally, we define key open questions and experimental priorities required to establish the temporal and causal relationships among astrocyte states. We argue that resolving these issues is essential for advancing therapeutic strategies that specifically target defined astrocyte phenotypes, rather than nonspecifically suppressing astrocyte activity, in aging and neurodegenerative diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41803335 · DOI · PMC12971753
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Aquaporin-4-dependent glymphatic solute transport in the rodent brain [4]
- Research article Astrocytes in the initiation and progression of epilepsy [5]
- Research article Neuroinflammation: An astrocyte perspective [6]
- Research article Astrocyte morphology [7]
- Research article Interactions of glial cells with neuronal synapses, from astrocytes to microglia and oligodendrocyte lineage cells [8]
- Research article Astrocyte Involvement in Blood-Brain Barrier Function: A Critical Update Highlighting Novel, Complex, Neurovascular Interactions [9]
References
- Bukalo O, O'Sullivan R, Tanisumi Y, Mendez A, Weinholtz C, Zimmerman S, et al.. Astrocytes enable amygdala neural representations supporting memory. . 2026. PMID 41673152 · DOI · PMC13061616
- Hein TM, Nespoli E, Hakani M, Wendt H, May SN, Jorzik J, et al.. NF-κB activation in astrocytes impairs wound healing after traumatic brain injury in male mice. . 2026. PMID 41792174 · DOI · PMC12976058
- Pacca-Corrêa JBL, Fernandes BM, Siqueira M, Schafbenker R, Baumart GJ, Damico IV, et al.. Astrocyte States in Brain Aging and Neurodegeneration: At the Crossroads of Senescence and Reactivity. . 2026. PMID 41803335 · DOI · PMC12971753
- Mestre H, Hablitz LM, Xavier AL, Feng W, Zou W, Pu T, et al.. Aquaporin-4-dependent glymphatic solute transport in the rodent brain. Elife. 2018. PMID 30561329 · DOI · PMC6307855
- Vezzani A, Ravizza T, Bedner P, Aronica E, Steinhäuser C, Boison D. Astrocytes in the initiation and progression of epilepsy. Nat Rev Neurol. 2022. PMID 36280704 · DOI · PMC10368155
- Lee HG, Lee JH, Flausino LE, Quintana FJ. Neuroinflammation: An astrocyte perspective. Sci Transl Med. 2023. PMID 37939162 · DOI
- Baldwin KT, Murai KK, Khakh BS. Astrocyte morphology. Trends Cell Biol. 2024. PMID 38180380 · DOI · PMC11590062
- Liu Y, Shen X, Zhang Y, Zheng X, Cepeda C, Wang Y, et al.. Interactions of glial cells with neuronal synapses, from astrocytes to microglia and oligodendrocyte lineage cells. Glia. 2023. PMID 36799296 · DOI
- Manu DR, Slevin M, Barcutean L, Forro T, Boghitoiu T, Balasa R. Astrocyte Involvement in Blood-Brain Barrier Function: A Critical Update Highlighting Novel, Complex, Neurovascular Interactions. Int J Mol Sci. 2023. PMID 38138976 · DOI · PMC10743219
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.