Evidence map›Paper›PMID 32709045›Full record

ReviewCells2020

Microglia: Agents of the CNS Pro-Inflammatory Response.

José A Rodríguez-Gómez, Edel Kavanagh, Pinelopi Engskog-Vlachos, Mikael K R Engskog, Antonio J Herrera, Ana M Espinosa-Oliva, Bertrand Joseph, Nabil Hajji, José L Venero, Miguel A Burguillos

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
220citing papers in PubMed, 2 pooled it
17.1field-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

220 citing papers in PubMed, 2 syntheses or guidelines pooled it, 348 citations in OpenAlex.

  1. Pooled it
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  7. β-Amyloid (Aβ) and Human Cathelicidin LL-37: Two Sides of the Same Coin?International journal of molecular sciences · 2026
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160 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

10 authors at 5 institutions in 3 countries.

José A Rodríguez-GómezInstitute of Biomedicine of Seville (IBIS)-Hospital Universitario Virgen del Rocío/CSIC/University of Seville, 41012 Seville, Spain.
Edel KavanaghDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, University of Seville, 41012 Seville, Spain.
Pinelopi Engskog-VlachosInstitute of Environmental Medicine, Toxicology Unit, Karolinska Institute, 17177 Stockholm, Sweden.
Mikael K R EngskogDepartment of Medicinal Chemistry, Analytical Pharmaceutical Chemistry, Uppsala University, 751 23 Uppsala, Sweden.
Antonio J HerreraInstitute of Biomedicine of Seville (IBIS)-Hospital Universitario Virgen del Rocío/CSIC/University of Seville, 41012 Seville, Spain.
Ana M Espinosa-OlivaInstitute of Biomedicine of Seville (IBIS)-Hospital Universitario Virgen del Rocío/CSIC/University of Seville, 41012 Seville, Spain.
Bertrand JosephInstitute of Environmental Medicine, Toxicology Unit, Karolinska Institute, 17177 Stockholm, Sweden.
Nabil HajjiDivision of Brain Sciences, The John Fulcher Molecular Neuro-Oncology Laboratory, Imperial College London, London W12 ONN, UK.
José L VeneroInstitute of Biomedicine of Seville (IBIS)-Hospital Universitario Virgen del Rocío/CSIC/University of Seville, 41012 Seville, Spain.ORCID 0000-0003-1137-8706
Miguel A BurguillosInstitute of Biomedicine of Seville (IBIS)-Hospital Universitario Virgen del Rocío/CSIC/University of Seville, 41012 Seville, Spain.
Instituto de Biomedicina de Sevilla · ESKarolinska Institutet · SEImperial College London · GBUniversidad de Sevilla · ESUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pro-inflammatory immune response driven by microglia is a key contributor to the pathogenesis of several neurodegenerative diseases. Though the research of microglia spans over a century, the last two decades have increased our understanding exponentially. Here, we discuss the phenotypic transformation from homeostatic microglia towards reactive microglia, initiated by specific ligand binding to pattern recognition receptors including toll-like receptor-4 (TLR4) or triggering receptors expressed on myeloid cells-2 (TREM2), as well as pro-inflammatory signaling pathways triggered such as the caspase-mediated immune response. Additionally, new research disciplines such as epigenetics and immunometabolism have provided us with a more holistic view of how changes in DNA methylation, microRNAs, and the metabolome may influence the pro-inflammatory response. This review aimed to discuss our current knowledge of pro-inflammatory microglia from different angles, including recent research highlights such as the role of exosomes in spreading neuroinflammation and emerging techniques in microglia research including positron emission tomography (PET) scanning and the use of human microglia generated from induced pluripotent stem cells (iPSCs). Finally, we also discuss current thoughts on the impact of pro-inflammatory microglia in neurodegenerative diseases.

Indexed as

AnimalsCaspasesCentral Nervous SystemEpigenesis, GeneticHumansInflammationMicrogliaModels, BiologicalCaspasescaspasesepigeneticsinflammationiPSCsmetabolomicsmicrogliaTLR4TREM2

Identifiers

PMID32709045
PMCPMC7407646
OpenAlexW3043443440

What OpenQuestion 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 OpenQuestion graph.