Evidence map›Paper›PMID 28811360›Full record

ArticlePhysiological reports2017

Involvement of midkine in the development of pulmonary fibrosis.

Kenichi Misa, Yoshinori Tanino, Xintao Wang, Takefumi Nikaido, Masami Kikuchi, Yuki Sato, Ryuichi Togawa, Mishie Tanino, Shinya Tanaka, Kenji Kadomatsu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 29% 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, 35 citations in OpenAlex.

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  10. Review
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  12. Article
  13. Midkine-A novel player in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  14. Article
  15. 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

11 authors at 3 institutions in 1 country.

Kenichi MisaDepartment of Pulmonary Medicine, Fukushima Medical University School of Medicine, Fukushima, Japan.
Yoshinori TaninoDepartment of Pulmonary Medicine, Fukushima Medical University School of Medicine, Fukushima, Japan ytanino@fmu.ac.jp.
Xintao WangDepartment of Pulmonary Medicine, Fukushima Medical University School of Medicine, Fukushima, Japan.
Takefumi NikaidoDepartment of Pulmonary Medicine, Fukushima Medical University School of Medicine, Fukushima, Japan.
Masami KikuchiDepartment of Pulmonary Medicine, Fukushima Medical University School of Medicine, Fukushima, Japan.
Yuki SatoDepartment of Pulmonary Medicine, Fukushima Medical University School of Medicine, Fukushima, Japan.
Ryuichi TogawaDepartment of Pulmonary Medicine, Fukushima Medical University School of Medicine, Fukushima, Japan.
Mishie TaninoDepartment of Cancer Pathology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Shinya TanakaDepartment of Cancer Pathology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Kenji KadomatsuDepartment of Biochemistry, Nagoya University School of Medicine, Nagoya, Japan.
Mitsuru MunakataDepartment of Pulmonary Medicine, Fukushima Medical University School of Medicine, Fukushima, Japan.
Fukushima Medical University · JPHokkaido University · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Midkine is a low-molecular-weight heparin-binding protein that is strongly expressed mainly in the midgestation period and has various physiological activities such as in development and cell migration. Midkine has been reported to be strongly expressed in cancer cells and in inflammation and repair processes, and to be involved in the pathogenesis of various diseases. However, its role in the lung is poorly understood. In this study, we analyzed the clinical characteristics of idiopathic pulmonary fibrosis patients in relation to midkine expression and used a mouse bleomycin-induced pulmonary fibrosis model to investigate the role of midkine in pulmonary fibrosis. In the idiopathic pulmonary fibrosis patients, the serum midkine level was significantly higher than in healthy subjects, and midkine levels in the serum and bronchoalveolar lavage (BAL) fluid correlated positively with the percentage of inflammatory cells in the BAL fluid. In wild-type mice, intratracheal bleomycin administration increased midkine expression in lung tissue. Additionally, compared with wild-type mice, midkine-deficient mice showed low expression of both collagen and

Indexed as

ActinsAdultAnimalsBronchoalveolar Lavage FluidCase-Control StudiesCollagenCytokinesFemaleHumansIdiopathic Pulmonary FibrosisLungLymphocyte CountMaleMiceMidkineTransforming Growth Factor betaActinsalpha-smooth muscle actin, mouseCollagenCytokinesMidkineTransforming Growth Factor betaTumor Necrosis Factor-alphaInflammationmidkinepulmonary fibrosisTGF‐β

Identifiers

PMID28811360
PMCPMC5582267
OpenAlexW2746354353

What OpenQuestion holds

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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.