Evidence map›Paper›PMID 34838047›Full record

ReviewJournal of neuroinflammation2021

Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation.

Erskine Chu, Richelle Mychasiuk, Margaret L Hibbs, Bridgette D Semple

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
9.6field-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

78 citing papers in PubMed, 138 citations in OpenAlex.

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  13. Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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18 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 1 country.

Erskine ChuDepartment of Immunology and Pathology, Central Clinical School, Monash University, Level 6, 89 Commercial Road, Melbourne, VIC, 3004, Australia.
Richelle MychasiukDepartment of Neuroscience, Central Clinical School, Monash University, Level 6, 99 Commercial Road, Melbourne, VIC, 3004, Australia.
Margaret L Hibbs *Department of Immunology and Pathology, Central Clinical School, Monash University, Level 6, 89 Commercial Road, Melbourne, VIC, 3004, Australia. Margaret.Hibbs@monash.edu.ORCID http://orcid.org/0000-0002-3751-6751
Bridgette D Semple *Department of Neuroscience, Central Clinical School, Monash University, Level 6, 99 Commercial Road, Melbourne, VIC, 3004, Australia. Bridgette.Semple@monash.edu.
Monash University · AUAlfred Health · AUThe Royal Melbourne Hospital · AU

Funding

department of education, skills and employment, australian government Research Training Stipend
6 · The paper itself

Abstract

Microglia are integral mediators of innate immunity within the mammalian central nervous system. Typical microglial responses are transient, intending to restore homeostasis by orchestrating the removal of pathogens and debris and the regeneration of damaged neurons. However, prolonged and persistent microglial activation can drive chronic neuroinflammation and is associated with neurodegenerative disease. Recent evidence has revealed that abnormalities in microglial signaling pathways involving phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) may contribute to altered microglial activity and exacerbated neuroimmune responses. In this scoping review, the known and suspected roles of PI3K-AKT signaling in microglia, both during health and pathological states, will be examined, and the key microglial receptors that induce PI3K-AKT signaling in microglia will be described. Since aberrant signaling is correlated with neurodegenerative disease onset, the relationship between maladapted PI3K-AKT signaling and the development of neurodegenerative disease will also be explored. Finally, studies in which microglial PI3K-AKT signaling has been modulated will be highlighted, as this may prove to be a promising therapeutic approach for the future treatment of a range of neuroinflammatory conditions.

Indexed as

AnimalsBrainHumansMicrogliaNeuroinflammatory DiseasesPhosphatidylinositol 3-KinaseSignal TransductionPhosphatidylinositol 3-KinaseAKTCell signalingGliaInnate immune systemNeurodegenerative diseasesPI3K

Identifiers

PMID34838047
PMCPMC8627624
OpenAlexW3217040496

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.