Evidence map›Paper›PMID 33020583›Full record

ArticleScientific reports2020

Spred2-deficiency enhances the proliferation of lung epithelial cells and alleviates pulmonary fibrosis induced by bleomycin.

Akina Kawara, Ryo Mizuta, Masayoshi Fujisawa, Toshihiro Ito, Chunning Li, Kaoru Nakamura, Cuiming Sun, Masaki Kuwabara, Masahiro Kitabatake, Teizo Yoshimura and 1 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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. SPRED2 Negatively Regulates CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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 2 institutions in 1 country.

Akina KawaraDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan.
Ryo MizutaDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan.
Masayoshi FujisawaDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan.
Toshihiro ItoDepartment of Immunology, Nara Medical University, Kashihara, 634-8521, Japan.
Chunning LiDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan.
Kaoru NakamuraDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan.
Cuiming SunDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan.
Masaki KuwabaraDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan.
Masahiro KitabatakeDepartment of Immunology, Nara Medical University, Kashihara, 634-8521, Japan.
Teizo YoshimuraDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan.ORCID http://orcid.org/0000-0002-3853-2075
Akihiro MatsukawaDepartment of Pathology and Experimental Medicine, Graduated School of Medicine, Dentistry and Pharmaceutical Science, Okayama University, 251 Shikata, Kita-ku, Okayama, 700-8558, Japan. amatsu@md.okayama-u.ac.jp.
Okayama University · JPNara Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitogen-activated protein kinase (MAPK) pathways are involved in many cellular processes, including the development of fibrosis. Here, we examined the role of Sprouty-related EVH-1-domain-containing protein (Spred) 2, a negative regulator of the MAPK-ERK pathway, in the development of bleomycin (BLM)-induced pulmonary fibrosis (PF). Compared to WT mice, Spred2

Indexed as

AnimalsBleomycinCell ProliferationCells, CulturedEpithelial CellsFibroblastsLipopolysaccharidesLungMacrophagesMAP Kinase Signaling SystemMiceMice, Inbred C57BLMyeloid CellsPulmonary FibrosisRepressor ProteinsTumor Necrosis Factor-alphaBleomycinLipopolysaccharidesRepressor ProteinsSpred2 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID33020583
PMCPMC7536438
OpenAlexW3089858188

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.