Evidence map›Paper›PMID 37382248›Full record

ArticleImmunity, inflammation and disease2023

YES-associated protein-regulated Smad7 worsen epithelial barrier injury of chronic sinusitis with nasal polyps.

Xiaocong Jiang, Longlan Shu, Yijun Liu, Yang Shen, Xia Ke, Jie Liu, Yucheng Yang

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

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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

7 citing papers in PubMed, 13 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

7 authors at 1 institution in 1 country.

Xiaocong JiangDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Longlan ShuDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.ORCID 0000-0002-0792-0761
Yijun LiuDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.ORCID 0000-0003-0125-6334
Yang ShenDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.ORCID 0000-0003-4714-0839
Xia KeDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.ORCID 0000-0003-2459-9612
Jie LiuDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.ORCID 0000-0003-3675-1845
Yucheng YangDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.ORCID 0000-0002-2413-2935
The Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic rhinosinusitis with nasal polyps (CRSwNP) was potentially due to the epithelial barrier injury. YES-associated protein (YAP) is a multifunctional transcriptional factor and plays versatile roles in the regulation and maintenance of epithelial barrier in different organs and tissues. The purpose of this study is to elucidate possible effect and mechanism of YAP on the epithelial barrier of CRSwNP.

methodsPatients were divided into CRSwNP group (n = 12) and control group (n = 9). The location of YAP, PDZ-binding transcriptional co-activator (TAZ), and Smad7 were estimated by immunohistochemistry and immunofluorescence. Meanwhile, the expression of YAP, TAZ, Zona occludens-1 (ZO-1), E-cadherin, and transforming growth factor-beta1 (TGF-β1) were detected by Western blot. After primary human nasal epithelial cells were treated with YAP inhibitor, the expression level of YAP, TAZ, ZO-1, E-cadherin, TGF-β1, and Smad7 were measured by Western blot.

resultsCompared with the control group, the protein levels of YAP, TAZ, and Smad7 were significantly upregulated, while TGF-β1, ZO-1, and E-cadherin were downregulated in CRSwNP. YAP and Smad7 demonstrated lower levels, while the expression of ZO-1, E-cadherin, and TGF-β1 rose slightly after YAP inhibitor treatment in primary nasal epithelial cells.

conclusionsHigher level of YAP may lead to CRSwNP epithelial barrier injury via the TGF-β1 signaling pathway, and the inhibition of YAP can partially reverse epithelial barrier function.

Indexed as

Nasal PolypsSinusitisSmad7 ProteinYAP-Signaling ProteinsCadherinsChronic DiseaseHumansTranscription FactorsTransforming Growth Factor beta1CadherinsSmad7 ProteinSMAD7 protein, humanTranscription FactorsTransforming Growth Factor beta1YAP1 protein, humanYAP-Signaling ProteinsCRSwNPnasal epithelial barrierSmad7TGF-β1YAP

Identifiers

PMID37382248
PMCPMC10266168
OpenAlexW4380685114

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Registered trials

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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.