Evidence map›Paper›PMID 25800044›Full record

ReviewBritish journal of pharmacology2016

Microglial M1/M2 polarization and metabolic states.

Ruben Orihuela, Christopher A McPherson, Gaylia Jean Harry

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,178 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,178citing papers in PubMed, 1 pooled it
40.2field-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

1,178 citing papers in PubMed, 1 synthesis or guideline pooled it, 2,002 citations in OpenAlex.

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  20. Journal of medical microbiology · 2026
    Article

1,118 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

3 authors at 2 institutions in 1 country.

Ruben OrihuelaNeurotoxicology Group, National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA.
Christopher A McPhersonNeurotoxicology Group, National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA.
Gaylia Jean HarryNeurotoxicology Group, National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA.
National Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Environmentally Induced Alterations In Neuron And Glia Development and AgingZIAES021164 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI HARRY, GAYLIA JEAN · 2009 to 2021
$15.4M
Neuroimmunotoxicology: autoimmunity, viral, infectious aZ01ES101623 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI HARRY, GAYLIA JEAN · 2003 to 2008
$2.8M
Environment Effects and Development of Neuron and GliaZ01ES021164 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI HARRY, GAYLIA JEAN · 1997 to 2008
$409k
"Mixtures of Xenoestrogens Alter Estradiol-induced Non-Genomic Signaling"F31ES021164 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI VINAS, RENE · 2012 to 2013
$40k
Intramural NIH HHS Z01 ES021164Intramural NIH HHS Z01 ES101623NIEHS NIH HHS ES021164NIEHS NIH HHS F31 ES021164
6 · The paper itself

Abstract

Microglia are critical nervous system-specific immune cells serving as tissue-resident macrophages influencing brain development, maintenance of the neural environment, response to injury and repair. As influenced by their environment, microglia assume a diversity of phenotypes and retain the capability to shift functions to maintain tissue homeostasis. In comparison with peripheral macrophages, microglia demonstrate similar and unique features with regards to phenotype polarization, allowing for innate immunological functions. Microglia can be stimulated by LPS or IFN-γ to an M1 phenotype for expression of pro-inflammatory cytokines or by IL-4/IL-13 to an M2 phenotype for resolution of inflammation and tissue repair. Increasing evidence suggests a role of metabolic reprogramming in the regulation of the innate inflammatory response. Studies using peripheral immune cells demonstrate that polarization to an M1 phenotype is often accompanied by a shift in cells from oxidative phosphorylation to aerobic glycolysis for energy production. More recently, the link between polarization and mitochondrial energy metabolism has been considered in microglia. Under these conditions, energy demands would be associated with functional activities and cell survival and thus, may serve to influence the contribution of microglia activation to various neurodegenerative conditions. This review examines the polarization states of microglia and their relationship to mitochondrial metabolism. Additional supporting experimental data are provided to demonstrate mitochondrial metabolic shifts in primary microglia and the BV-2 microglia cell line induced under LPS (M1) and IL-4/IL-13 (M2) polarization.

Indexed as

AnimalsHumansInflammationInterleukin-13Interleukin-4LipopolysaccharidesMicrogliaMitochondriaPhenotypeInterleukin-13Interleukin-4Lipopolysaccharides

Identifiers

PMID25800044
PMCPMC4742299
OpenAlexW1768846296

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.