Evidence map›Paper›PMID 30510259›Full record

ArticleScientific reports2018

Ninjurin1 Plays a Crucial Role in Pulmonary Fibrosis by Promoting Interaction between Macrophages and Alveolar Epithelial Cells.

Seungho Choi, Jong Kyu Woo, Yeong-Su Jang, Ju-Hee Kang, Jong-Ik Hwang, Je Kyung Seong, Yeo Sung Yoon, Seung Hyun Oh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-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

30 citing papers in PubMed, 65 citations in OpenAlex.

  1. NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026
    Review
  2. The role of NINJ1 in diseases.Cell death discovery · 2026
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  19. Ninjurin1 Deletion in NG2-Positive Pericytes Prevents Microvessel Maturation and Delays Wound Healing.JID innovations : skin science from molecules to population health · 2022
    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

8 authors at 3 institutions in 2 countries.

Seungho ChoiCollege of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0002-8313-6290
Jong Kyu WooKorea Mouse Phenotyping Center, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Yeong-Su JangCollege of Pharmacy, Gachon University, Incheon, Republic of Korea.
Ju-Hee KangCollege of Pharmacy, Gachon University, Incheon, Republic of Korea.
Jong-Ik HwangGraduate School of Medicine, Korea University, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0002-0729-1782
Je Kyung SeongKorea Mouse Phenotyping Center, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Yeo Sung YoonCollege of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea. ysyoon@snu.ac.kr.
Seung Hyun OhCollege of Pharmacy, Gachon University, Incheon, Republic of Korea. eyeball@hanmail.net.
Seoul National University · KRGachon University · KRKorea University · KR

Funding

National Research Foundation of Korea (NRF) NRF-2016M3A9D5A01953817
6 · The paper itself

Abstract

The transmembrane nerve injury-induced protein 1 (Ninjurin1 or Ninj1) is involved in progressing inflammatory diseases. In this study, we aimed to investigate a novel function of Ninj1 in pulmonary fibrosis. We found that the expression of Ninj1 in a patient cohort was upregulated in the lung specimens of idiopathic pulmonary fibrosis patients as well as mice with bleomycin-induced pulmonary fibrosis. In addition, the BLM-injected Ninj1 KO mice exhibited a mild fibrotic phenotype, as compared to WT mice. Therefore, we hypothesized that Ninj1 would play an important role in the development of pulmonary fibrosis. We discovered that Ninj1 expression increased in BLM-treated macrophages and alveolar epithelial cells (AECs). Interestingly, macrophages bound to BLM-treated AECs were activated. However, when Ninj1 expression was suppressed in either of AECs or macrophages, contact-dependent activation of macrophages with AECs was diminished. In addition, introduction of recombinant mouse Ninj1

Indexed as

AnimalsCell Adhesion Molecules, NeuronalEpithelial CellsMacrophages, AlveolarMiceMice, KnockoutNerve Growth FactorsPulmonary AlveoliPulmonary FibrosisRespiratory MucosaCell Adhesion Molecules, NeuronalNerve Growth FactorsNinj1 protein, mouse

Identifiers

PMID30510259
PMCPMC6277454
OpenAlexW2902000408

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.