Evidence map›Paper›PMID 34169527›Full record

ReviewJournal of neurochemistry2021

Potential crosstalk between sonic hedgehog-WNT signaling and neurovascular molecules: Implications for blood-brain barrier integrity in autism spectrum disorder.

Evelyne Gozal, Rekha Jagadapillai, Jun Cai, Gregory N Barnes

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of neurochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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  16. Exploring key genes and pathways associated with sex differences in autism spectrum disorder: integrated bioinformatic analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
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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

4 authors at 1 institution in 1 country.

Evelyne GozalDepartment of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, KY, USA.ORCID 0000-0001-7451-087X
Rekha JagadapillaiDepartment of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, KY, USA.
Jun CaiDepartment of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, KY, USA.
Gregory N BarnesDepartment of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, KY, USA.ORCID 0000-0002-7711-5506
University of Louisville · US

Funding

University of Louisville Center for Integrative Environmental Health SciencesP30ES030283 · NIEHS · UNIVERSITY OF LOUISVILLE · PI Amanda Jo LeBlanc · 2020 to 2026
$10.0M
NIEHS NIH HHS P30 ES030283
6 · The paper itself

Abstract

Autism Spectrum Disorder (ASD) is a neurodevelopmental disease originating from combined genetic and environmental factors. Post-mortem human studies and some animal ASD models have shown brain neuroinflammation, oxidative stress, and changes in blood-brain barrier (BBB) integrity. However, the signaling pathways leading to these inflammatory findings and vascular alterations are currently unclear. The BBB plays a critical role in controlling brain homeostasis and immune response. Its dysfunction can result from developmental genetic abnormalities or neuroinflammatory processes. In this review, we explore the role of the Sonic Hedgehog/Wingless-related integration site (Shh/Wnt) pathways in neurodevelopment, neuroinflammation, and BBB development. The balance between Wnt-β-catenin and Shh pathways controls angiogenesis, barriergenesis, neurodevelopment, central nervous system (CNS) morphogenesis, and neuronal guidance. These interactions are critical to maintain BBB function in the mature CNS to prevent the influx of pathogens and inflammatory cells. Genetic mutations of key components of these pathways have been identified in ASD patients and animal models, which correlate with the severity of ASD symptoms. Disruption of the Shh/Wnt crosstalk may therefore compromise BBB development and function. In turn, impaired Shh signaling and glial activation may cause neuroinflammation that could disrupt the BBB. Elucidating how ASD-related mutations of Shh/Wnt signaling could cause BBB leaks and neuroinflammation will contribute to our understanding of the role of their interactions in ASD pathophysiology. These observations may provide novel targeted therapeutic strategies to prevent or alleviate ASD symptoms while preserving normal developmental processes. Cover Image for this issue: https://doi.org/10.1111/jnc.15081.

Indexed as

AnimalsAutism Spectrum DisorderBlood-Brain BarrierHedgehog ProteinsHumansMutationNeurovascular CouplingTight JunctionsWnt Signaling PathwayHedgehog Proteinsautismblood brain barrierendothelial injurymicroglianeuroinflammationWnt-Hedgehog

Identifiers

PMID34169527
PMCPMC8484047
OpenAlexW3177370284

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.