Evidence map›Paper›PMID 31868203›Full record

ArticleBioscience reports2020

Bleomycin induces epithelial-to-mesenchymal transition via bFGF/PI3K/ESRP1 signaling in pulmonary fibrosis.

Chang-Mei Weng, Qing Li, Kui-Jun Chen, Cheng-Xiong Xu, Meng-Sheng Deng, Tao Li, Dong-Dong Zhang, Zhao-Xia Duan, Zhi-Qiang Chen, Guan-Hua Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 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

12 authors at 1 institution in 1 country.

Chang-Mei WengResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Qing LiCancer Center, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Kui-Jun ChenResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Cheng-Xiong XuCancer Center, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Meng-Sheng DengResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Tao LiJoint Surgery Center, Southwest Hospital, Army Medical University, Chongqing 400038, China.
Dong-Dong ZhangResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Zhao-Xia DuanResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Zhi-Qiang ChenResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Guan-Hua LiResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Jing ChenResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Jian-Min WangResearch Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, People's Republic of China.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a fatal and chronic disease with a high rate of infection and mortality; however, its etiology and pathogenesis remain unclear. Studies have revealed that epithelial-mesenchymal transition (EMT) is a crucial cellular event in IPF. Here, we identified that the pulmonary fibrosis inducer bleomycin simultaneously increased the expression of bFGF and TGF-β1 and inhibited epithelial-specific regulatory protein (ESRP1) expression in vivo and in vitro. In addition, in vitro experiments showed that bFGF and TGF-β1 down-regulated the expression of ESRP1 and that silencing ESRP1 promoted EMT in A549 cells. Notably, we determined that bFGF activates PI3K/Akt signaling, and treatment with the PI3K/Akt inhibitor LY294002 inhibited bleomycin-induced cell morphology changes and EMT. In addition, the effects of LY294002 on bleomycin-induced EMT were inhibited by ESRP1 silencing in A549 cells. Taken together, these findings suggest that bleomycin induced EMT through down-regulating ESRP1 by simultaneously increasing bFGF and TGF-β1 in pulmonary fibrosis. Additionally, our findings indicated that bFGF inhibits ESRP1 by activating PI3K/Akt signaling.

Indexed as

BleomycinEpithelial-Mesenchymal TransitionA549 CellsAnimalsDisease Models, AnimalFibroblast Growth Factor 2Gene Expression RegulationHumansIdiopathic Pulmonary FibrosisLungMaleMicePhosphatidylinositol 3-KinaseRNA-Binding ProteinsSignal TransductionTransforming Growth Factor beta1BleomycinESRP1 protein, humanESRP1 protein, mouseFibroblast Growth Factor 2Phosphatidylinositol 3-KinaseRNA-Binding ProteinsTGFB1 protein, humanTgfb1 protein, mouseTransforming Growth Factor beta1bFGFBleomycinEMTPI3K/Akt SignalingPulmonary Fibrosis

Identifiers

PMID31868203
PMCPMC6960066
OpenAlexW2997819974

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.