Evidence map›Paper›PMID 8515840›Full record

ReviewNeuroscience1993

Molecular profile of reactive astrocytes--implications for their role in neurologic disease.

M Eddleston, L Mucke

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 332 papers.

0numbers the graph read from it
0cells of the map it votes in
332citing papers in PubMed
42.9field-weighted citation impact, top 1% of its field
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

332 citing papers in PubMed, 1,429 citations in OpenAlex.

  1. Galectin-related protein, a key contributor, drives diabetes-associated neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  5. Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025
    Review
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  8. CaFrontiers in cellular neuroscience · 2025
    Review
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272 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

2 authors at 1 institution in 1 country.

M EddlestonDepartment of Neuropharmacology, Scripps Research Institute.
L Mucke
Scripps Research Institute · US

Funding

THE ROLE OF CYTOKINES IN THE PATHOGENESIS OF AIDS DEMENTIA COMPLEXP50MH047680 · NIMH · SCRIPPS RESEARCH INSTITUTE · PI BLOOM, FLOYD ELLIOTT · 1990 to 2000
$77k
NIMH NIH HHS MHA47680
6 · The paper itself

Abstract

The central nervous system responds to diverse neurologic injuries with a vigorous activation of astrocytes. While this phenomenon is found in many different species, its function is obscure. Understanding the molecular profile characteristic of reactive astrocytes should help define their function. The purpose of this review is to provide a summary of molecules whose levels of expression differentiate activated from resting astrocytes and to use the molecular profile of reactive astrocytes as the basis for speculations on the functions of these cells. At present, reactive astrocytosis is defined primarily as an increase in the number and size of cells expressing glial fibrillary acidic protein. In vivo, this increase in glial fibrillary acidic protein-positive cells reflects predominantly phenotypic changes of resident astroglia rather than migration or proliferation of such cells. Upon activation, astrocytes upmodulate the expression of a large number of molecules. From this molecular profile it becomes apparent that reactive astrocytes may benefit the injured nervous system by participating in diverse biological processes. For example, upregulation of proteases and protease inhibitors could help remodel the extracellular matrix, regulate the concentration of different proteins in the neuropil and clear up debris from degenerating cells. Cytokines are key mediators of immunity and inflammation and could play a critical role in the regulation of the blood-central nervous system interface. Neurotrophic factors, transporter molecules and enzymes involved in the metabolism of excitotoxic amino acids or in the antioxidant pathway may help protect neurons and other brain cells by controlling neurotoxin levels and contributing to homeostasis within the central nervous system. Therefore, an impairment of astroglial performance has the potential to exacerbate neuronal dysfunction. Based on the synopsis of studies presented, a number of issues become apparent that deserve a more extensive analysis. Among them are the relative contribution of microglia and astrocytes to early wound repair, the characterization of astroglial subpopulations, the specificity of the astroglial response in different diseases as well as the analysis of reactive astrocytes with techniques that can resolve fast physiologic processes. Differences between reactive astrocytes in vivo and primary astrocytes in culture are discussed and underline the need for the development and exploitation of models that will allow the analysis of reactive astrocytes in the intact organism.

Indexed as

Antibody FormationAstrocytesHumansMaleNerve Growth FactorsNerve Tissue ProteinsNervous System DiseasesNeurotoxinsRestNerve Growth FactorsNerve Tissue ProteinsNeurotoxins

Identifiers

PMID8515840
PMCPMC7130906
OpenAlexW2006289803

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.