Evidence map›Paper›PMID 37828019›Full record

ReviewSignal transduction and targeted therapy2023

Astrocytes in human central nervous system diseases: a frontier for new therapies.

Alexei Verkhratsky, Arthur Butt, Baoman Li, Peter Illes, Robert Zorec, Alexey Semyanov, Yong Tang, Michael V Sofroniew

Abstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 256 papers.

0numbers the graph read from it
0cells of the map it votes in
256citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

256 citing papers in PubMed.

  1. Article
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  11. Review
  12. The role of dopamine decline, astrocyte reactivity and cerebral small-vessel disease in cognitive aging.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Article
  13. Article
  14. Article
  15. Perisynaptic Astrocytic Processes as Communication Hubs and Early Sites of Dysfunction.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2026
    Review
  16. Article
  17. Neuroprotective Potential ofBiomolecules · 2026
    Article
  18. Article
  19. Article
  20. Article

196 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Alexei VerkhratskyInternational Joint Research Centre on Purinergic Signalling/School of Health and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, China. Alexej.Verkhratsky@manchester.ac.uk.ORCID http://orcid.org/0000-0003-2592-9898
Arthur ButtInstitute of Biomedical and Biomolecular Sciences, School of Pharmacy and Biomedical Sciences, University of Portsmouth, Portsmouth, UK.
Baoman LiDepartment of Forensic Analytical Toxicology, School of Forensic Medicine, China Medical University, Shenyang, China.
Peter IllesInternational Joint Research Centre on Purinergic Signalling/School of Health and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Robert ZorecCelica Biomedical, Lab Cell Engineering, Technology Park, 1000, Ljubljana, Slovenia.
Alexey SemyanovDepartment of Physiology, Jiaxing University College of Medicine, 314033, Jiaxing, China.
Yong TangInternational Joint Research Centre on Purinergic Signalling/School of Health and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, China. tangyong@cdutcm.edu.cn.ORCID http://orcid.org/0000-0002-2543-066X
Michael V SofroniewDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. sofroniew@mednet.ucla.edu.ORCID http://orcid.org/0000-0001-6075-0178

Funding

Injectable biomaterial depots to manipulate scar and foster axon growth after SCIR01NS084030 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SOFRONIEW, MICHAEL V · 2014 to 2023
$3.0M
NINDS NIH HHS R01 NS084030
6 · The paper itself

Abstract

Astroglia are a broad class of neural parenchymal cells primarily dedicated to homoeostasis and defence of the central nervous system (CNS). Astroglia contribute to the pathophysiology of all neurological and neuropsychiatric disorders in ways that can be either beneficial or detrimental to disorder outcome. Pathophysiological changes in astroglia can be primary or secondary and can result in gain or loss of functions. Astroglia respond to external, non-cell autonomous signals associated with any form of CNS pathology by undergoing complex and variable changes in their structure, molecular expression, and function. In addition, internally driven, cell autonomous changes of astroglial innate properties can lead to CNS pathologies. Astroglial pathophysiology is complex, with different pathophysiological cell states and cell phenotypes that are context-specific and vary with disorder, disorder-stage, comorbidities, age, and sex. Here, we classify astroglial pathophysiology into (i) reactive astrogliosis, (ii) astroglial atrophy with loss of function, (iii) astroglial degeneration and death, and (iv) astrocytopathies characterised by aberrant forms that drive disease. We review astroglial pathophysiology across the spectrum of human CNS diseases and disorders, including neurotrauma, stroke, neuroinfection, autoimmune attack and epilepsy, as well as neurodevelopmental, neurodegenerative, metabolic and neuropsychiatric disorders. Characterising cellular and molecular mechanisms of astroglial pathophysiology represents a new frontier to identify novel therapeutic strategies.

Indexed as

Central Nervous System DiseasesStrokeAstrocytesHomeostasisHumans

Identifiers

PMID37828019
PMCPMC10570367

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.