Evidence map›Paper›PMID 25025333›Full record

ArticlePloS one2014

Genetic targets of hydrogen sulfide in ventilator-induced lung injury--a microarray study.

Sashko Spassov, Dietmar Pfeifer, Karl Strosing, Stefan Ryter, Matthias Hummel, Simone Faller, Alexander Hoetzel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Gene Expression Analysis to Assess the Relevance of Rodent Models to Human Lung Injury.American journal of respiratory cell and molecular biology · 2017
    Pooled it
  2. Utility of NO and HNitric oxide : biology and chemistry · 2022
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. HIntensive care medicine experimental · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Working with nitric oxide and hydrogen sulfide in biological systems.American journal of physiology. Lung cellular and molecular physiology · 2015
    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

7 authors at 2 institutions in 2 countries.

Sashko SpassovDepartment of Anaesthesiology and Intensive Care Medicine, University Medical Center Freiburg, Freiburg, Germany.
Dietmar PfeiferGenomics Core Lab, Dept. Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Freiburg, Germany.
Karl StrosingDepartment of Anaesthesiology and Intensive Care Medicine, University Medical Center Freiburg, Freiburg, Germany.
Stefan RyterJoan and Sanford I. Weill Department of Medicine, New York-Presbyterian Hospital, Weill Cornell Medical College, New York, New York, United States of America.
Matthias HummelDepartment of Anaesthesiology and Intensive Care Medicine, University Medical Center Freiburg, Freiburg, Germany.
Simone FallerDepartment of Anaesthesiology and Intensive Care Medicine, University Medical Center Freiburg, Freiburg, Germany.
Alexander HoetzelDepartment of Anaesthesiology and Intensive Care Medicine, University Medical Center Freiburg, Freiburg, Germany.
University Medical Center Freiburg · DECornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, we have shown that inhalation of hydrogen sulfide (H2S) protects against ventilator-induced lung injury (VILI). In the present study, we aimed to determine the underlying molecular mechanisms of H2S-dependent lung protection by analyzing gene expression profiles in mice. C57BL/6 mice were subjected to spontaneous breathing or mechanical ventilation in the absence or presence of H2S (80 parts per million). Gene expression profiles were determined by microarray, sqRT-PCR and Western Blot analyses. The association of Atf3 in protection against VILI was confirmed with a Vivo-Morpholino knockout model. Mechanical ventilation caused a significant lung inflammation and damage that was prevented in the presence of H2S. Mechanical ventilation favoured the expression of genes involved in inflammation, leukocyte activation and chemotaxis. In contrast, ventilation with H2S activated genes involved in extracellular matrix remodelling, angiogenesis, inhibition of apoptosis, and inflammation. Amongst others, H2S administration induced Atf3, an anti-inflammatory and anti-apoptotic regulator. Morpholino mediated reduction of Atf3 resulted in elevated lung injury despite the presence of H2S. In conclusion, lung protection by H2S during mechanical ventilation is associated with down-regulation of genes related to oxidative stress and inflammation and up-regulation of anti-apoptotic and anti-inflammatory genes. Here we show that Atf3 is clearly involved in H2S mediated protection.

Indexed as

AnimalsGene Expression ProfilingHydrogen SulfideLung InjuryMaleMiceMice, Inbred C57BLVentilator-Induced Lung InjuryHydrogen Sulfide

Identifiers

PMID25025333
PMCPMC4099342
OpenAlexW2006512241

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.