Evidence map›Paper›PMID 22052925›Full record

ReviewProceedings of the American Thoracic Society2011

Involvement of ceramide in cell death responses in the pulmonary circulation.

Irina Petrache, Daniela N Petrusca, Russell P Bowler, Krzysztof Kamocki

Open access · greenAbstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Peripheral blood mononuclear cell gene expression in chronic obstructive pulmonary disease.American journal of respiratory cell and molecular biology · 2013
    Trial
  3. Article
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  6. Review
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  8. Article
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  10. Review
  11. Article
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  16. Review
  17. Article
  18. Review
  19. Sphingolipids as cell fate regulators in lung development and disease.Apoptosis : an international journal on programmed cell death · 2015
    Review
  20. Plasma sphingolipids associated with chronic obstructive pulmonary disease phenotypes.American journal of respiratory and critical care medicine · 2015
    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

4 authors at 3 institutions in 1 country.

Irina PetracheDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Indiana University, Indianapolis, Indiana, USA. ipetrach@iupui.edu
Daniela N Petrusca
Russell P Bowler
Krzysztof Kamocki
National Jewish Health · USIndiana University – Purdue University Indianapolis · USPulmonary and Critical Care Associates · US

Funding

Ceramide-induced Lung Destruction in EmphysemaR01HL077328 · NHLBI · NATIONAL JEWISH HEALTH · PI PETRACHE, IRINA · 2006 to 2024
$8.0M
EMAP II, a molecular link of inflammation and apoptosis in pulmonary emphysema.R01HL090950 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CLAUSS, MATTHIAS, PETRACHE, IRINA · 2008 to 2011
$1.5M
Molecular mechanism of alveolar injury caused by cigarette smokeR21DA029249 · NIDA · INDIANA UNIVERSITY INDIANAPOLIS · PI PETRACHE, IRINA · 2010 to 2011
$418k
Signaling Sphingolipids in COPDR03HL095440 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BERDYSHEV, EVGENY V, PETRACHE, IRINA · 2008 to 2009
$169k
NHLBI NIH HHS R01 HL077328NHLBI NIH HHS R01 HL090950NHLBI NIH HHS R03 HL095440NIDA NIH HHS R21 DA029249NIDA NIH HHS R21 DA029249-01
6 · The paper itself

Abstract

Ceramides are signaling sphingolipids involved in cellular homeostasis but also in pathological processes such as unwanted apoptosis, growth arrest, oxidative stress, or senescence. Several enzymatic pathways are responsible for the synthesis of ceramides, which can be activated in response to exogenous stimuli such as cytokines, radiation, or oxidative stress. Endothelial cells are particularly rich in acid sphingomyelinases, which can be rapidly activated to produce ceramides, both intracellular and at the plasma membrane. In addition, neutral sphingomyelinases, the de novo pathway and the ceramide recycling pathway, may generate excessive ceramides involved in endothelial cell responses. When up-regulated, ceramides trigger signaling pathways that culminate in endothelial cell death, which in murine lungs has been linked to the development of emphysema-like disease. Furthermore, ceramides may be released paracellularly where they are believed to exert paracrine activities. Such effects, along with ceramides released by inflammatory mediators, may contribute to lung inflammation and pulmonary edema, because ceramide-challenged pulmonary endothelial cells exhibit decreased barrier function, independent of apoptosis. Reestablishing the sphingolipid homeostasis, either by modulating ceramide synthesis or by opposing its biological effects through augmentation of the prosurvival sphingosine-1 phosphate, may alleviate acute or chronic pulmonary conditions characterized by vascular endothelial cell death or dysfunction.

Indexed as

ApoptosisAnimalsCeramidesDisease Models, AnimalHumansLungMiceMicrocirculationPulmonary CirculationPulmonary EmphysemaCeramides

Identifiers

PMID22052925
PMCPMC3359077
OpenAlexW2139171483

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.