Evidence map›Paper›PMID 22140070›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

Activation of calpains mediates early lung neutrophilic inflammation in ventilator-induced lung injury.

Dejie Liu, Zhibo Yan, Richard D Minshall, David E Schwartz, Yuguo Chen, Guochang Hu

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. In Vivo Calpain Knockdown Using Delivery of siRNA.Methods in molecular biology (Clifton, N.J.) · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016
    Review
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Dejie LiuDepartment of Pharmacology, University of Illinois College of Medicine, Chicago, 60612, USA.
Zhibo Yan
Richard D Minshall
David E Schwartz
Yuguo Chen
Guochang Hu
Qilu Hospital of Shandong University · CNUniversity of Illinois Chicago · US

Funding

Role Of p120 Catenin In Sepsis-Induced Lung InjuryR01HL104092 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI HU, GUOCHANG · 2010 to 2020
$3.9M
NHLBI NIH HHS 5R01HL104092
6 · The paper itself

Abstract

Lung inflammatory responses in the absence of infection are considered to be one of primary mechanisms of ventilator-induced lung injury. Here, we determined the role of calpain in the pathogenesis of lung inflammation attributable to mechanical ventilation. Male C57BL/6J mice were subjected to high (28 ml/kg) tidal volume ventilation for 2 h in the absence and presence of calpain inhibitor I (10 mg/kg). To address the isoform-specific functions of calpain 1 and calpain 2 during mechanical ventilation, we utilized a liposome-based delivery system to introduce small interfering RNAs targeting each isoform in pulmonary vasculature in vivo. Mechanical ventilation with high tidal volume induced rapid (within minutes) and persistent calpain activation and lung inflammation as evidenced by neutrophil recruitment, production of TNF-α and IL-6, pulmonary vascular hyperpermeability, and lung edema formation. Pharmaceutical calpain inhibition significantly attenuated these inflammatory responses caused by lung hyperinflation. Depletion of calpain 1 or calpain 2 had a protective effect against ventilator-induced lung inflammatory responses. Inhibition of calpain activity by means of siRNA silencing or pharmacological inhibition also reduced endothelial nitric oxide (NO) synthase (NOS-3)-mediated NO production and subsequent ICAM-1 phosphorylation following high tidal volume ventilation. These results suggest that calpain activation mediates early lung inflammation during ventilator-induced lung injury via NOS-3/NO-dependent ICAM-1 phosphorylation and neutrophil recruitment. Inhibition of calpain activation may therefore provide a novel and promising strategy for the prevention and treatment of ventilator-induced lung injury.

Indexed as

Neutrophil InfiltrationAnimalsCalpainEnzyme ActivationGene Knockdown TechniquesGlycoproteinsInflammationIntercellular Adhesion Molecule-1LungMaleMiceMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIIPhosphorylationRNA InterferenceCalpaincalpain inhibitorsCapn1 protein, mouseCapn2 protein, mouseGlycoproteinsIntercellular Adhesion Molecule-1Nitric OxideNitric Oxide Synthase Type IIINos3 protein, mouse

Identifiers

PMID22140070
PMCPMC3289265
OpenAlexW2106319656

What OpenQuestion holds

Textmetadata
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.