Evidence map›Paper›PMID 32587339›Full record

ArticleScientific reports2020

Growth Factor Midkine Aggravates Pulmonary Arterial Hypertension via Surface Nucleolin.

Daisuke Kinoshita, Tetsuro Shishido, Tetsuya Takahashi, Miyuki Yokoyama, Takayuki Sugai, Ken Watanabe, Harutoshi Tamura, Satoshi Nishiyama, Hiroki Takahashi, Takanori Arimoto and 9 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Pulmonary Vascular Remodeling in Pulmonary Hypertension.Journal of personalized medicine · 2023
    Review
  14. Article
  15. Article
  16. Midkine-A novel player in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  17. Review
  18. 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

19 authors at 4 institutions in 2 countries.

Daisuke KinoshitaThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Tetsuro ShishidoThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan. tshishid@med.id.yamagata-u.ac.jp.
Tetsuya TakahashiThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Miyuki YokoyamaThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Takayuki SugaiThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Ken WatanabeThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Harutoshi TamuraThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Satoshi NishiyamaThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Hiroki TakahashiThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Takanori ArimotoThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Takuya MiyamotoThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Tetsu WatanabeThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Satoshi KishidaDepartment of Biochemistry, Nagoya University Graduate School of Medicine, Aichi, Japan.
Kenji KadomatsuDepartment of Biochemistry, Nagoya University Graduate School of Medicine, Aichi, Japan.
Jun-Ichi AbeDepartment of Cardiology - Research, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, US.
Yasuchika TakeishiDepartment of Cardiology and Hematology, Fukushima Medical University, Fukushima, Japan.
Tsuneo KontaThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Isao KubotaThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Masafumi WatanabeThe Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Yamagata University · JPNagoya University · JPFukushima Medical University · JPThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a progressive fatal disease caused by pulmonary arterial remodeling. Midkine regulates cell proliferation and migration, and it is induced by hypoxia, but its roles in pulmonary arterial remodeling remain unclear. Serum midkine levels were significantly increased in PAH patients compared with control patients. Midkine expression was increased in lungs and sera of hypoxia-induced PAH mice. Hypoxia-induced pulmonary arterial remodeling and right ventricular hypertrophy were attenuated in midkine-knockout mice. Midkine-induced proliferation and migration of pulmonary arterial smooth muscle cells (PASMC) and epidermal growth factor receptor (EGFR) signaling were significantly increased under hypoxia, which also induced cell-surface translocation of nucleolin. Nucleolin siRNA treatment suppressed midkine-induced EGFR activation in vitro, and nucleolin inhibitor AS1411 suppressed proliferation and migration of PASMC induced by midkine. Furthermore, AS1411 significantly prevented the development of PAH in Sugen hypoxia rat model. Midkine plays a crucial role in PAH development through interaction with surface nucleolin. These data define a role for midkine in PAH development and suggest midkine-nucleolin-EGFR axis as a novel therapeutic target for PAH.

Indexed as

AgedAnimalsAptamers, NucleotideCell MembraneCell MovementCell NucleusCell ProliferationCells, CulturedDisease Models, AnimalErbB ReceptorsFemaleHumansHypoxiaLungMaleMiceAGRO 100Aptamers, NucleotideEGFR protein, humanEGFR protein, mouseErbB ReceptorsMDK protein, humanMdk protein, mouseMdk protein, ratMidkineNucleolinOligodeoxyribonucleotidesPhosphoproteinsRNA-Binding Proteins

Identifiers

PMID32587339
PMCPMC7316741
OpenAlexW3037964775

What OpenQuestion holds

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LicenceCC BY
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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.