Evidence map›Paper›PMID 38041162›Full record

ArticleBiological research2023

Role of SYVN1 in the control of airway remodeling in asthma protection by promoting SIRT2 ubiquitination and degradation.

Bing Dai, Si Liu, Wenxin Shen, Li Chen, Qianlan Zhou, Lina Han, Qinzhen Zhang, Lishen Shan

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

Article in Biological research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

1 citing paper in PubMed, 9 citations in OpenAlex.

  1. Article
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

8 authors at 1 institution in 1 country.

Bing Dai *Department of Pediatrics, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Shenyang, 110004, China.
Si Liu *Department of Pediatrics, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Shenyang, 110004, China.
Wenxin ShenDepartment of Pediatrics, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Shenyang, 110004, China.
Li ChenDepartment of Pediatrics, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Shenyang, 110004, China.
Qianlan ZhouDepartment of Pediatrics, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Shenyang, 110004, China.
Lina HanDepartment of Pediatrics, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Shenyang, 110004, China.
Qinzhen ZhangDepartment of Pediatrics, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Shenyang, 110004, China.
Lishen ShanDepartment of Pediatrics, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Shenyang, 110004, China. shanls@sj-hospital.org.
China Medical University · CN

Funding

Basic Scientific Research Project of Colleges and Universities of Liaoning Province, General Program No. LJKZ0746Basic Scientific Research Project of Colleges and Universities of Liaoning Province, Key Program No. LJKZ0746
6 · The paper itself

Abstract

backgroundAsthma is a heterogenous disease that characterized by airway remodeling. SYVN1 (Synoviolin 1) acts as an E3 ligase to mediate the suppression of endoplasmic reticulum (ER) stress through ubiquitination and degradation. However, the role of SYVN1 in the pathogenesis of asthma is unclear.

resultsIn the present study, an ovalbumin (OVA)-induced murine model was used to evaluate the effect of SYVN1 on asthma. An increase in SYVN1 expression was observed in the lungs of mice after OVA induction. Overexpression of SYVN1 attenuated airway inflammation, goblet cell hyperplasia and collagen deposition induced by OVA. The increased ER stress-related proteins and altered epithelial-mesenchymal transition (EMT) markers were also inhibited by SYVN1 in vivo. Next, TGF-β1-induced bronchial epithelial cells (BEAS-2B) were used to induce EMT process in vitro. Results showed that TGF-β1 stimulation downregulated the expression of SYVN1, and SYVN1 overexpression prevented ER stress response and EMT process in TGF-β1-induced cells. In addition, we identified that SYVN1 bound to SIRT2 and promoted its ubiquitination and degradation. SIRT2 overexpression abrogated the protection of SYVN1 on ER stress and EMT in vitro.

conclusionsThese data suggest that SYVN1 suppresses ER stress through the ubiquitination and degradation of SIRT2 to block EMT process, thereby protecting against airway remodeling in asthma.

Indexed as

AsthmaTransforming Growth Factor beta1Airway RemodelingAnimalsEpithelial-Mesenchymal TransitionMiceSirtuin 2UbiquitinationUbiquitin-Protein LigasesSirt2 protein, mouseSirtuin 2Syvn1 protein, mouseTransforming Growth Factor beta1Ubiquitin-Protein LigasesAsthmaEndoplasmic reticulum stressEpithelial-mesenchymal transitionSIRT2SYVN1Ubiquitination

Identifiers

PMID38041162
PMCPMC10693155
OpenAlexW4389257709

What OpenQuestion holds

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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.