Evidence map›Paper›PMID 25821552›Full record

ArticleOxidative medicine and cellular longevity2015

Enhancement of the acrolein-induced production of reactive oxygen species and lung injury by GADD34.

Yang Sun, Sachiko Ito, Naomi Nishio, Yuriko Tanaka, Nana Chen, Lintao Liu, Ken-ichi Isobe

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. 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
1.7field-weighted citation impact, top 17% 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.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. HidroxAntioxidants (Basel, Switzerland) · 2021
    Article
  11. Article
  12. The integrated stress response in pulmonary disease.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  13. Article
  14. Hesperetin mitigates acrolein-induced apoptosis in lung cells in vitro and in vivo.Redox report : communications in free radical research · 2018
    Article
  15. Acrolein Exposure in Hookah Smokers and Non-Smokers Exposed to Hookah Tobacco Secondhand Smoke: Implications for Regulating Hookah Tobacco Products.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Preventive and therapeutic effects ofAvicenna journal of phytomedicine
    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

7 authors at 2 institutions in 2 countries.

Yang SunDepartment of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan ; Department of Immunology, Norman Bethune College of Medicine, Jilin University, Changchun 130021, China.
Sachiko ItoDepartment of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Naomi NishioDepartment of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yuriko TanakaDepartment of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Nana ChenDepartment of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Lintao LiuDepartment of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000-0002-7984-194X
Ken-ichi IsobeDepartment of Immunology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Nagoya University · JPFirst Bethune Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by lung destruction and inflammation. As a major compound of cigarette smoke, acrolein plays a critical role in the induction of respiratory diseases. GADD34 is known as a growth arrest and DNA damage-related gene, which can be overexpressed in adverse environmental conditions. Here we investigated the effects of GADD34 on acrolein-induced lung injury. The intranasal exposure of acrolein induced the expression of GADD34, developing the pulmonary damage with inflammation and increase of reactive oxygen species (ROS). Conversely, the integrality of pulmonary structure was preserved and the generation of ROS was reduced in GADD34-knockout mice. Acrolein-induced phosphorylation of eIF2α in GADD34-knockout epithelial cells by shRNA protected cell death by reducing misfolded protein-caused oxidative stress. These data indicate that GADD34 participates in the development of acrolein-induced lung injury.

Indexed as

AcetylcysteineAcroleinAnimalsApoptosisCells, CulturedEndoplasmic Reticulum StressEpithelial CellsFemaleInflammationLungLung InjuryMiceMice, Inbred C57BLMice, KnockoutPhosphorylationProtein Phosphatase 1AcetylcysteineAcroleineIF2alpha kinase, mousePpp1r15a protein, mouseProtein Phosphatase 1Protein Serine-Threonine KinasesReactive Oxygen SpeciesRNA, Small Interfering

Identifiers

PMID25821552
PMCPMC4364366
OpenAlexW2033920136

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.