Evidence map›Paper›PMID 30195261›Full record

ReviewGlia2018

How to reprogram microglia toward beneficial functions.

Marta Fumagalli, Marta Lombardi, Pierre Gressens, Claudia Verderio

Open access · hybridAbstract readReview
In one paragraph

Review in Glia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

72 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
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  15. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
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  19. Article
  20. Article

12 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

4 authors at 3 institutions in 3 countries.

Marta FumagalliDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, via Balzaretti, 9 -20133, Milan, Italy.
Marta LombardiIRCCS Humanitas, via Manzoni 56, 20089, Rozzano, Italy.
Pierre GressensPROTECT, INSERM, Université Paris Diderot, Sorbonne Paris Cité, 1141 Paris, France.
Claudia VerderioIRCCS Humanitas, via Manzoni 56, 20089, Rozzano, Italy.ORCID 0000-0001-7216-5873
Humanitas University · ITSt Thomas' Hospital · GBUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia, brain cells of nonneural origin, orchestrate the inflammatory response to diverse insults, including hypoxia/ischemia or maternal/fetal infection in the perinatal brain. Experimental studies have demonstrated the capacity of microglia to recognize pathogens or damaged cells activating a cytotoxic response that can exacerbate brain damage. However, microglia display an enormous plasticity in their responses to injury and may also promote resolution stages of inflammation and tissue regeneration. Despite the critical role of microglia in brain pathologies, the cellular mechanisms that govern the diverse phenotypes of microglia are just beginning to be defined. Here we review emerging strategies to drive microglia toward beneficial functions, selectively reporting the studies which provide insights into molecular mechanisms underlying the phenotypic switch. A variety of approaches have been proposed which rely on microglia treatment with pharmacological agents, cytokines, lipid messengers, or microRNAs, as well on nutritional approaches or therapies with immunomodulatory cells. Analysis of the molecular mechanisms relevant for microglia reprogramming toward pro-regenerative functions points to a central role of energy metabolism in shaping microglial functions. Manipulation of metabolic pathways may thus provide new therapeutic opportunities to prevent the deleterious effects of inflammatory microglia and to control excessive inflammation in brain disorders.

Indexed as

AnimalsCellular ReprogrammingEncephalitisHumansMicrogliabeneficial phenotypemetabolismmicrogliamiRNAre-program

Identifiers

PMID30195261
PMCPMC6585737
OpenAlexW2892002213

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.