Evidence map›Paper›PMID 31692229›Full record

ArticleJournal of cellular and molecular medicine2020

A new FGFR inhibitor disrupts the TGF-β1-induced fibrotic process.

Mi-Hyoung Kim, Seung-Youn Jung, Kyung-Hee Song, Jeong-In Park, Jiyeon Ahn, Eun-Ho Kim, Jong Kuk Park, Sang-Gu Hwang, Hee-Jong Woo, Jie-Young Song

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

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  5. Chronic Kidney Disease-associated Lung Injury Is Mediated by Phosphate-induced MAPK/AKT Signaling.American journal of respiratory cell and molecular biology · 2024
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  16. A new FGFR inhibitor disrupts the TGF-β1-induced fibrotic process.Journal of cellular and molecular medicine · 2020
    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

10 authors.

Mi-Hyoung KimDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Seung-Youn JungDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Kyung-Hee SongDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Jeong-In ParkDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Jiyeon AhnDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Eun-Ho KimDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Jong Kuk ParkDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Sang-Gu HwangDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.
Hee-Jong WooLaboratory of Immunology, College of Veterinary Medicine, Seoul National University, Seoul, Korea.
Jie-Young SongDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.ORCID 0000-0002-5769-3886

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis (PF) is chronic and irreversible damage to the lung characterized by fibroblast activation and matrix deposition. Although recently approved novel anti-fibrotic agents can improve the lung function and survival of patients with PF, the overall outcomes remain poor. In this study, a novel imidazopurine compound, 3-(2-chloro-6-fluorobenzyl)-1,6,7-trimethyl-1H-imidazo[2,1-f]purine-2,4(3H,8H)-dione (IM-1918), markedly inhibited transforming growth factor (TGF)-β-stimulated reporter activity and reduced the expression of representative fibrotic markers, such as connective tissue growth factor, fibronectin, collagen and α-smooth muscle actin, on human lung fibroblasts. However, IM-1918 neither decreased Smad-2 and Smad-3 nor affected p38MAPK and JNK. Instead, IM-1918 reduced Akt and extracellular signal-regulated kinase 1/2 phosphorylation increased by TGF-β. Additionally, IM-1918 inhibited the phosphorylation of fibroblast growth factor receptors 1 and 3. In a bleomycin-induced murine lung fibrosis model, IM-1918 profoundly reduced fibrotic areas and decreased collagen and α-smooth muscle actin accumulation. These results suggest that IM-1918 can be applied to treat lung fibrosis.

Indexed as

AnimalsAntibiotics, AntineoplasticBleomycinEnzyme InhibitorsFibronectinsImidazolesMaleMiceMice, Inbred C57BLPulmonary FibrosisReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 3Transforming Growth Factor betaAntibiotics, AntineoplasticBleomycinEnzyme InhibitorsFibronectinsFN1 protein, humanImidazolesReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 3Transforming Growth Factor betaAktextracellular signal-regulated kinase 1/2fibroblast growth factor receptorimidazopurinelung fibrosistransforming growth factor-β

Identifiers

PMID31692229
PMCPMC6933341

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.