Evidence map›Paper›PMID 36543124›Full record

ArticleCell reports2022

IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury.

Guanxi Xiao, Rosie Kumar, Yutaro Komuro, Jasmine Burguet, Visesha Kakarla, Ida Azizkhanian, Sunil A Sheth, Christopher K Williams, Xinhai R Zhang, Michal Macknicki and 9 more

Open access · goldFull text read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  3. Routes of precursors' migration in remyelination.Brain : a journal of neurology · 2026
    Review
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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

19 authors at 5 institutions in 2 countries.

Guanxi XiaoDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Rosie KumarDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Yutaro KomuroDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Jasmine BurguetInstitut Jean-Pierre Bourgin, INRA, AgroParisTech, CNRS, Université Paris-Saclay, 78000 Versailles, France.
Visesha KakarlaDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Ida AzizkhanianNew York Medical College, School of Medicine, Valhalla, NY, USA.
Sunil A ShethDepartment of Neurology, UT Health McGovern School of Medicine, Houston, TX, USA.
Christopher K WilliamsDepartment of Neuropathology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Xinhai R ZhangDepartment of Neuropathology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Michal MacknickiDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Andrew BrummDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Riki KawaguchiDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; Department of Psychiatry, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA, USA.
Phu MaiDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Naoki KanekoDepartment of Radiological Sciences, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Harry V VintersDepartment of Neuropathology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
S Thomas CarmichaelDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Leif A HavtonDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; Department of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Charles DeCarliDepartment of Neurology, University of California, Davis, Davis, CA, USA.
Jason D HinmanDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. Electronic address: jhinman@mednet.ucla.edu.
University of California, Los Angeles · USCentre National de la Recherche Scientifique · FRNew York Medical College · USThe University of Texas Health Science Center at Houston · USUniversity of California, Davis · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Mechanisms for vascular regulation of remyelination in white matter injuryRF1NS114336 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HINMAN, JASON D · 2020 to 2024
$2.0M
Molecular Mechanisms of Axonal Degeneration After White Matter StrokeK08NS083740 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HINMAN, JASON D · 2013 to 2017
$831k
NIA NIH HHS P30 AG010129NIDDK NIH HHS P30 DK041301NINDS NIH HHS K08 NS083740NINDS NIH HHS RF1 NS114336
6 · The paper itself

Abstract

Cerebral small vessel disease and brain white matter injury are worsened by cardiovascular risk factors including obesity. Molecular pathways in cerebral endothelial cells activated by chronic cerebrovascular risk factors alter cell-cell signaling, blocking endogenous and post-ischemic white matter repair. Using cell-specific translating ribosome affinity purification (RiboTag) in white matter endothelia and oligodendrocyte progenitor cells (OPCs), we identify a coordinated interleukin-chemokine signaling cascade within the oligovascular niche of subcortical white matter that is triggered by diet-induced obesity (DIO). DIO induces interleukin-17B (IL-17B) signaling that acts on the cerebral endothelia through IL-17Rb to increase both circulating and local endothelial expression of CXCL5. In white matter endothelia, CXCL5 promotes the association of OPCs with the vasculature and triggers OPC gene expression programs regulating cell migration through chemokine signaling. Targeted blockade of IL-17B reduced vessel-associated OPCs by reducing endothelial CXCL5 expression. In multiple human cohorts, blood levels of CXCL5 function as a diagnostic and prognostic biomarker of vascular cognitive impairment.

Indexed as

Brain InjuriesWhite MatterAnimalsBrainChemokine CXCL5Endothelial CellsHumansInterleukin-17MiceOligodendrogliaSignal TransductionChemokine CXCL5CXCL5 protein, humanInterleukin-17cerebral small vessel diseaseCP: ImmunologyCP: NeuroscienceCXCL5high-fat dietIL-17inflammationobesitystrokewhite matter

Identifiers

PMID36543124
PMCPMC10026849
OpenAlexW4312084893

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read50
identifiers read1
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.