Evidence map›Paper›PMID 33549109›Full record

ArticleRespiratory research2021

Role of CXCL16 in BLM-induced epithelial-mesenchymal transition in human A549 cells.

Zhenzhen Ma, Chunyan Ma, Qingfeng Zhang, Yang Bai, Kun Mu, Xiangyuan Liu, Qingrui Yang

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
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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 3 institutions in 1 country.

Zhenzhen MaDepartment of Rheumatology and Immunology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Chunyan MaDepartment of Rheumatology and Immunology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Qingfeng ZhangDepartment of Rheumatology and Immunology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Yang BaiDepartment of Rheumatology and Immunology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Kun MuDepartment of Pathology, Qilu Hospital, Shandong University, Jinan, 250012, China.
Xiangyuan Liu *Department of Rheumatology and Immunology, Peking University Third Hospital, Beijing, 100191, China. liu-xiangyuan@263.net.
Qingrui Yang *Department of Rheumatology and Immunology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China. qryang720@163.com.ORCID http://orcid.org/0000-0001-6433-4745
Shandong University · CNPeking University · CNQilu Hospital of Shandong University · CN

Funding

Key Technology Research and Development Program of Shandong (CN) 2017GSF18134National Natural Science Foundation of China 81671605National Natural Science Foundation of China 81771744
6 · The paper itself

Abstract

Alveolar epithelial cells play an essential role in the initiation and progression of pulmonary fibrosis, and the occurrence of epithelial-mesenchymal transition (EMT) may be the early events of pulmonary fibrosis. Recent studies have shown chemokines are involved in the complex process of EMT, and CXC chemokine ligand 16 (CXCL16) is also associated with many fibrosis-related diseases. However, whether CXCL16 is dysregulated in alveolar epithelial cells and the role of CXCL16 in modulating EMT in pulmonary fibrosis has not been reported. In this study, we found that CXCL16 and its receptor C-X-C motif chemokine receptor 6 (CXCR6) were upregulated in bleomycin induced EMT in human alveolar type II-like epithelial A549 cells. Synergistic effect of CXCL16 and bleomycin in promoting EMT occurrence, extracellular matrix (ECM) excretion, as well as the pro-inflammatory and pro-fibrotic cytokines productions in A549 cells were observed, and those biological functions were impaired by CXCL16 siRNA. We further confirmed that CXCL16 regulated EMT in A549 cells via the TGF-β1/Smad3 pathways. These results indicated that CXCL16 could promote pulmonary fibrosis by promoting the process of EMT via the TGF-β1/Smad3 signaling pathway.

Indexed as

A549 CellsAntibiotics, AntineoplasticBleomycinChemokine CXCL16Dose-Response Relationship, DrugEpithelial-Mesenchymal TransitionHumansAntibiotics, AntineoplasticBleomycinChemokine CXCL16CXCL16 protein, humanChemokinesCXCL16Epithelial–mesenchymal transitionPulmonary fibrosis

Identifiers

PMID33549109
PMCPMC7866482
OpenAlexW3128836702

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.