Evidence map›Paper›PMID 29138212›Full record

ArticleBiology open2017

Bax-inhibiting peptide attenuates bleomycin-induced lung injury in mice.

Kunihiro Suzuki, Toyoshi Yanagihara, Tetsuya Yokoyama, Takashige Maeyama, Saiko Ogata-Suetsugu, Masako Arimura-Omori, Hironori Mikumo, Naoki Hamada, Eiji Harada, Kazuyoshi Kuwano and 2 more

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Amyloid-beta glycation induces neuronal mitochondrial dysfunction and Alzheimer's pathogenesis via VDAC1-dependent mtDNA efflux.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Physiological and pharmacological modulation of BAX.Trends in pharmacological sciences · 2022
    Review
  5. Review
  6. Curcumin protects murine lung mesenchymal stem cells from HThe Journal of international medical research · 2020
    Article
  7. Review
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

12 authors at 2 institutions in 1 country.

Kunihiro SuzukiResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Toyoshi YanagiharaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan yanagiha@kokyu.med.kyushu-u.ac.jp.ORCID http://orcid.org/0000-0002-2212-0631
Tetsuya YokoyamaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Takashige MaeyamaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Saiko Ogata-SuetsuguResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Masako Arimura-OmoriResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Hironori MikumoResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Naoki HamadaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Eiji HaradaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Kazuyoshi KuwanoDivision of Respiratory Diseases, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Taishi HaradaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Yoichi NakanishiResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Kyushu University · JPJikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bax is a pro-apoptotic member of the Bcl-2 family of proteins, and plays a central role in mitochondria-dependent apoptosis. Several lines of evidence have implied that Bax is involved in both epithelial apoptosis and fibroblast proliferation in idiopathic pulmonary fibrosis; however, the mechanisms remain unknown. Bax-inhibiting peptide V5 (BIP-V5) exhibits membrane permeability and inhibits the activation of Bax.The purpose of this study was to investigate whether the control of Bax activity by BIP-V5 reduces the degree of bleomycin-induced lung injury. C57BL/6J mice were administered bleomycin and BIP-V5 intratracheally on day 0. Bronchoalveolar lavage fluid and lung tissue were obtained on day 7. Human pulmonary alveolar epithelial cells (A549 cells) and mouse pulmonary alveolar epithelial cells (LA-4 cells) were stimulated with bleomycin to induce apoptosis.Administration of BIP-V5 improved the survival rate and degree of bleomycin-induced lung injury by suppressing Bax activation in mice. BIP-V5 treatment decreased bleomycin-induced apoptosis of alveolar epithelial cell lines (A549 cells and LA-4 cells) by suppressing Bax activation. These results indicate that administration of BIP-V5 may constitute a novel therapeutic strategy against lung injury.

Indexed as

ApoptosisBaxLung injury

Identifiers

PMID29138212
PMCPMC5769644
OpenAlexW2768157957

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.