Evidence map›Paper›PMID 29219210›Full record

ReviewGlia2018

Bioenergetic regulation of microglia.

Soumitra Ghosh, Erika Castillo, Elma S Frias, Raymond A Swanson

Abstract 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 172 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
172citing papers in PubMed, 2 pooled it
8.1field-weighted citation impact, top 2% 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

172 citing papers in PubMed, 2 syntheses or guidelines pooled it, 286 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
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  5. Review
  6. Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026
    Article
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112 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 1 institution in 1 country.

Soumitra GhoshDepartment of Neurology, University of California San Francisco, San Francisco, CA.
Erika CastilloDepartment of Neurology, University of California San Francisco, San Francisco, CA.
Elma S FriasDepartment of Neurology, University of California San Francisco, San Francisco, CA.
Raymond A SwansonDepartment of Neurology, University of California San Francisco, San Francisco, CA.ORCID 0000-0002-3664-5359
San Francisco VA Medical Center · US

Funding

Regulatory Control of Glutamate - Induced Superoxide Production [Admin Supplement]R01NS081149 · NINDS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI SWANSON, RAYMOND A · 2012 to 2016
$1.7M
Thiol repletion therapy for Parkinson's diseaseI01BX003249 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI SWANSON, RAYMOND A · 2017 to 2020
–
BLRD VA I01 BX003249NINDS NIH HHS R01 NS081149
6 · The paper itself

Abstract

Microglia have diverse actions, ranging from synapse pruning in development to cytotoxic effects in disease. Brain energy metabolism and substrate availability vary under normal and disease states, but how these variations influence microglial function is relatively unknown. Microglia, like most other cell types, express the full complement of gene products required for both glycolytic and oxidative metabolism. Evidence suggests that microglia increase aerobic glycolysis and decrease respiration when activated by various stimuli. Mitochondrial function, glucose availability, and glycolytic rate influence pro-inflammatory gene expression at both transcriptional and post-translational levels. These effects are mediated through CtBP, an NADH-sensitive transcriptional co-repressor; through effects on NLRP3 inflammasome assembly and caspase-1 activation; through formation of advanced glycation end-products; and by less well-defined mechanisms. In addition to these transcriptional effects, microglial glucose metabolism is also required for superoxide production by NADPH oxidase, as glucose is the obligate substrate for regenerating NADPH in the hexose monophosphate shunt. Microglia also metabolize acetoacetate and β-hydroxybutyrate, which are generated during fasting or ketogenic diet, and respond to these ketones as metabolic signals. β-Hydroxybutyrate inhibits histone de-acetylases and activates microglial GRP109A receptors. These actions suppress microglia activation after brain injury and promote neuroprotective microglia phenotypes. As our understanding of microglial activation matures, additional links between energy metabolism and microglial function are likely to be identified.

Indexed as

AnimalsEnergy MetabolismHumansMicrogliaglycolysisinflammasomeketonesuperoxideTREM2

Identifiers

PMID29219210
PMCPMC5903989
OpenAlexW2773698836

What OpenQuestion holds

Textmetadata
LicenceTDM
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.