Evidence map›Paper›PMID 38003682›Full record

ReviewInternational journal of molecular sciences2023

The Role of Atypical Chemokine Receptors in Neuroinflammation and Neurodegenerative Disorders.

Hunter G Lindsay, Colby J Hendrix, Josue D Gonzalez Murcia, Christopher Haynie, K Scott Weber

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

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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.

Hunter G LindsayDepartment of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA.ORCID 0000-0003-0549-353X
Colby J HendrixDepartment of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA.
Josue D Gonzalez MurciaDepartment of Neurobiology, University of Utah, Salt Lake City, UT 84112, USA.ORCID 0000-0003-2951-8316
Christopher HaynieDepartment of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA.
K Scott WeberDepartment of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA.ORCID 0000-0003-3688-2191
Brigham Young University · USUniversity of Utah · US

Funding

BYU Gerontology Center grant No grant numberJames Bobbitt Research Grant No grant number
6 · The paper itself

Abstract

Neuroinflammation is associated with several neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Neuroinflammation provides protection in acute situations but results in significant damage to the nervous system if chronic. Overexpression of chemokines within the brain results in the recruitment and activation of glial and peripheral immune cells which can propagate a cascading inflammatory response, resulting in neurodegeneration and the onset of neurodegenerative disorders. Recent work has identified the role of atypical chemokine receptors (ACKRs) in neurodegenerative conditions. ACKRs are seven-transmembrane domain receptors that do not follow canonical G protein signaling, but regulate inflammatory responses by modulating chemokine abundance, location, and availability. This review summarizes what is known about the four ACKRs and three putative ACKRs within the brain, highlighting their known expression and discussing the current understanding of each ACKR in the context of neurodegeneration. The ability of ACKRs to alter levels of chemokines makes them an appealing therapeutic target for neurodegenerative conditions. However, further work is necessary to understand the expression of several ACKRs within the neuroimmune system and the effectiveness of targeted drug therapies in the prevention and treatment of neurodegenerative conditions.

Indexed as

Neurodegenerative DiseasesReceptors, ChemokineChemokinesHumansNeuroinflammatory DiseasesSignal TransductionChemokinesReceptors, Chemokineatypical chemokine receptorschemokinescytokinesneurodegenerative disordersneuroinflammation

Identifiers

PMID38003682
PMCPMC10671188
OpenAlexW4388795756

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.