Evidence map›Paper›PMID 26677863›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

Inhibition of EGF Receptor Blocks the Development and Progression of Peritoneal Fibrosis.

Li Wang, Na Liu, Chongxiang Xiong, Liuqing Xu, Yingfeng Shi, Andong Qiu, Xiujuan Zang, Haiping Mao, Shougang Zhuang

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 62 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Li WangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China;
Na LiuDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China;
Chongxiang XiongDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China;
Liuqing XuDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China;
Yingfeng ShiDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China;
Andong QiuSchool of Life Science and Technology, Advanced Institute of Translational Medicine, Tongji University, Shanghai, China;
Xiujuan ZangDepartment of Nephrology, Shanghai Songjiang District Central Hospital, Shanghai, China;
Haiping MaoDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Providence, China; and.
Shougang ZhuangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China; Department of Medicine, Rhode Island Hospital and Alpert School of Medicine, Brown University, Providence, Rhode Island szhuang@lifespan.org.
Shanghai East Hospital · CNSongjiang District Central Hospital · CNSun Yat-sen University · CNTongji University · CN

Funding

Histone deacetylases as novel therapeutic targets for kidney fibrosisR01DK085065 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2010 to 2017
$2.8M
NIDDK NIH HHS R01 DK085065
6 · The paper itself

Abstract

Inhibitors of EGF receptor (EGFR) have antifibrotic effects in several organs, but the effect of these inhibitors on the development of peritoneal fibrosis is unknown. Here, we explored the therapeutic effect of gefitinib, a specific inhibitor of EGFR, on the development and progression of peritoneal fibrosis in a rat model. Daily intraperitoneal injections of chlorhexidine gluconate induced peritoneal fibrosis, indicated by thickening of the submesothelial area with an accumulation of collagen fibrils and activation of myofibroblasts, accompanied by time-dependent phosphorylation of EGFR. Administration of gefitinib immediately after injury prevented the onset of peritoneal fibrosis and delayed administration after the onset of peritoneal fibrosis halted fibrosis progression. Gefitinib treatment abrogated the increased phosphorylation of EGFR, Smad3, signal transducer and activator of transcription 3, and NF-κB during peritoneal fibrosis; it also inhibited the accompanying overproduction of TGF-β1 and proinflammatory cytokines and the infiltration of macrophages to the injured peritoneum. Moreover, gefitinib significantly reduced the peritoneal increase of CD31-positive blood vessels and vascular EGF-positive cells after injury. Finally, gefitinib also attenuated high glucose-induced peritoneal fibrosis in rats and abrogated TGF-β1-induced phosphorylation of Smad3 and the epithelial-to-mesenchymal transition of cultured human peritoneal mesothelial cells. These results demonstrate that EGFR contributes to peritoneal fibrosis, inflammation, and angiogenesis, suggesting that EGFR inhibitors may have therapeutic potential in attenuating peritoneal fibrosis.

Indexed as

AnimalsDisease ProgressionErbB ReceptorsGefitinibMalePeritoneal FibrosisPhosphorylationQuinazolinesRatsRats, Sprague-DawleyTime FactorsTransforming Growth Factor beta1ErbB ReceptorsGefitinibQuinazolinesTransforming Growth Factor beta1epidermal growth factorfibrosisperitoneal dialysissignalingTGF-betaVEGF

Identifiers

PMID26677863
PMCPMC5004637
OpenAlexW2232955085

What OpenQuestion holds

Textmetadata
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.