Evidence map›Paper›PMID 29724997›Full record

ArticleCell death & disease2018

Epithelial cell-derived cytokines CST3 and GDF15 as potential therapeutics for pulmonary fibrosis.

Young-Im Kim, Hyun-Woo Shin, Yang-Sook Chun, Chung-Hyun Cho, Jaemoon Koh, Doo Hyun Chung, Jong-Wan Park

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

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  19. The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  20. Enhanced Proliferation of Ly6CJournal of immunology (Baltimore, Md. : 1950) · 2021
    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

7 authors at 2 institutions in 2 countries.

Young-Im KimDepartment of Biomedical Sciences, BK21-plus Education Program, Seoul National University College of Medicine, Seoul, Korea.
Hyun-Woo ShinDepartment of Biomedical Sciences, BK21-plus Education Program, Seoul National University College of Medicine, Seoul, Korea.ORCID 0000-0002-4038-9992
Yang-Sook ChunDepartment of Biomedical Sciences, BK21-plus Education Program, Seoul National University College of Medicine, Seoul, Korea.
Chung-Hyun ChoDepartment of Biomedical Sciences, BK21-plus Education Program, Seoul National University College of Medicine, Seoul, Korea.
Jaemoon KohDepartment of Pathology, Seoul National University Hospital, Seoul, Korea.
Doo Hyun ChungDepartment of Biomedical Sciences, BK21-plus Education Program, Seoul National University College of Medicine, Seoul, Korea.
Jong-Wan ParkDepartment of Biomedical Sciences, BK21-plus Education Program, Seoul National University College of Medicine, Seoul, Korea. parkjw@snu.ac.kr.ORCID 0000-0003-4676-5191
Seoul National University · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While wound healing is completed, the epithelium functions to normalize the interstitial context by eliminating fibroblasts excited during matrix reconstruction. If not, tissues undergo pathologic fibrosis. Pulmonary fibrosis is a fatal and hardly curable disorder. We here tried to identify epithelium-derived cytokines capable of ameliorating pulmonary fibrosis. Human lung fibroblasts were inactivated in epithelial cell-conditioned media. Cystatin C (CST3) and growth differentiation factor 15 (GDF15) were found to be enriched in the conditioned media and to inhibit the growth and activation of lung fibroblasts by inactivating the TGF-Smad pathway. In mouse and human lungs with interstitial fibrosis, CST3 and GDF15 expressions were markedly reduced, and the restoration of these cytokines alleviated the fibrotic changes in mouse lungs. These results suggest that CST3 and GDF15 are bona fide regulators to prevent excessive proliferation and activation of fibroblasts in injured lungs. These cytokines could be potential therapeutics for ameliorating interstitial lung fibrosis.

Indexed as

A549 CellsAnimalsBleomycinCell ProliferationCystatin CCytokinesEpithelial CellsFibroblastsGene Expression ProfilingGene Expression RegulationGrowth Differentiation Factor 15HCT116 CellsHumansIdiopathic Pulmonary FibrosisLungLung Diseases, InterstitialBleomycinCST3 protein, humanCystatin CCytokinesGDF15 protein, humanGrowth Differentiation Factor 15Receptor, Transforming Growth Factor-beta Type ISmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTGFBR1 protein, human

Identifiers

PMID29724997
PMCPMC5938700
OpenAlexW2801196888

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.