Evidence map›Paper›PMID 30554385›Full record

ReviewMolecular neurobiology2019

Microglia Receptors in Animal Models of Traumatic Brain Injury.

Daniel Younger, Madhuvika Murugan, Kakulavarapu V Rama Rao, Long-Jun Wu, Namas Chandra

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Impact Induces Phagocytic Defect in Reactive Microglia.bioRxiv : the preprint server for biology · 2025
    Article
  5. Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Interleukin-1 Receptor Antagonist as Therapy for Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

5 authors at 2 institutions in 1 country.

Daniel Younger *Department of Bioengineering, New Jersey Institute of Technology, 111 Lock Street, Room105 CHEN bldg, Newark, NJ, 07102, USA.
Madhuvika Murugan *Department of Bioengineering, New Jersey Institute of Technology, 111 Lock Street, Room105 CHEN bldg, Newark, NJ, 07102, USA.
Kakulavarapu V Rama RaoDepartment of Bioengineering, New Jersey Institute of Technology, 111 Lock Street, Room105 CHEN bldg, Newark, NJ, 07102, USA.
Long-Jun WuDepartment of Neurology, Mayo Clinic, Rochester, MN, 55905, USA.
Namas ChandraDepartment of Bioengineering, New Jersey Institute of Technology, 111 Lock Street, Room105 CHEN bldg, Newark, NJ, 07102, USA. namas.chandra@njit.edu.ORCID http://orcid.org/0000-0003-4804-4523
New Jersey Institute of Technology · USMayo Clinic · US

Funding

Medical Research and Materiel Command W81XWH-15-1-0303New Jersey Commission on Brain Injury Research CBIR17PIL020Rutgers, The State University of New Jersey BHI-RUN-NJIT-2016
6 · The paper itself

Abstract

Microglia have been implicated as a key mediator of chronic inflammation following traumatic brain injury (TBI). The animal models of TBI vary significantly based on the type of brain injury (focal versus diffuse). This has made it extremely difficult to assess the role of microglia and the window of microglia activation. Hence, the focus of this review is to summarize the time course of microglia activation in various animal models of TBI. The review explores the repertoire of secondary injury mechanisms such as aberrant neurotransmitter release, oxidative stress, blood-brain barrier disruption, and production of pro-inflammatory cytokines that follow microglia activation. Since receptors act as sensors for activation, we highlight certain microglia receptors that have been implicated in TBI pathology, including fractalkine receptor (CX3CR1), purinergic receptor (P2Y12R), Toll-like receptor (TLR4), scavenger receptors, tumor necrosis factor receptor (TNF-1R), interleukin receptor (IL-1R), complement receptors, and peroxisome proliferator-activated receptor (PPAR). In addition to describing their downstream signaling pathways in TBI, we describe the functional consequences of their activation and the implication in behavioral outcomes. Taken together, this review will provide a holistic view of the role of microglia and its receptors in TBI based on animal studies.

Indexed as

Disease Models, AnimalAnimalsBrain Injuries, TraumaticHumansMicrogliaOxidative StressReactive Oxygen SpeciesReceptors, Cell SurfaceReactive Oxygen SpeciesReceptors, Cell SurfaceBrain injuryMicrogliaReceptors

Identifiers

PMID30554385
OpenAlexW2904164379

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.