Evidence map›Paper›PMID 19428331›Full record

ReviewBiochemical pharmacology2009

Regulators of endothelial and epithelial barrier integrity and function in acute lung injury.

Rudolf Lucas, Alexander D Verin, Stephen M Black, John D Catravas

Abstract readReview
In one paragraph

Review in Biochemical pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
12.8field-weighted citation impact, top 1% 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

127 citing papers in PubMed, 287 citations in OpenAlex.

  1. Trial
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  10. Redox mechanisms of environmental toxicants on male reproductive function.Frontiers in cell and developmental biology · 2024
    Review
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  20. International journal of molecular sciences · 2022
    Article

67 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Rudolf LucasVascular Biology Center, Medical College of Georgia, Augusta, GA 30912-2500, USA. rlucas@mcg.edu
Alexander D Verin
Stephen M Black
John D Catravas
Augusta University · US

Funding

Microtubules in lung endothelial cell barrier regulationR01HL067307 · NHLBI · UNIVERSITY OF CHICAGO · PI VERIN, ALEXANDER D · 2001 to 2009
$2.5M
Protective activity of the lectin-like domain of TNF in permeability edemaR01HL094609 · NHLBI · AUGUSTA UNIVERSITY · PI LUCAS, RUDOLF · 2010 to 2013
$1.5M
ATP in Lung Endothelial Barrier EnhancementR01HL083327 · NHLBI · UNIVERSITY OF CHICAGO · PI VERIN, ALEXANDER D · 2006 to 2009
$1.5M
NHLBI NIH HHS R01 HL067307NHLBI NIH HHS R01 HL083327NHLBI NIH HHS R01 HL094609
6 · The paper itself

Abstract

Permeability edema is a life-threatening complication accompanying acute lung injury (ALI), severe pneumonia and the acute respiratory distress syndrome (ARDS), which can be associated with a reduced alveolar liquid clearance (ALC) capacity, a disruption of the alveolar epithelial barrier, and an increased capillary endothelial permeability. Bacterial and viral infections can directly promote pulmonary endothelial hyperpermeability and indirectly decrease the function and/or expression of ion transporters regulating ALC in type II alveolar epithelial cells, by means of inducing a strong inflammatory and oxidative stress response in the infected lungs. Apart from ventilation strategies, no standard treatment exists for permeability edema, making the search for novel regulators of endothelial and epithelial hyperpermeability and dysfunction important. Here, we present an overview of recently identified substances that inhibit and/or reverse endothelial barrier disruption and permeability or alveolar epithelial dysfunction: (1) zinc chelators, which were shown to attenuate the effects of oxidative stress on the pulmonary endothelium; (2) peroxisome proliferator activated receptor (PPAR) ligands, which have been shown to exert anti-inflammatory effects, by decreasing the expression of pro-inflammatory genes; (3) extracellular ATP, produced during inflammation, which induces a rapid and dose-dependent increase in transendothelial electrical resistance (TER) across pulmonary endothelial cells; (4) the lectin-like domain of TNF, which is spatially distinct from the receptor binding sites and which protects from hydrostatic and permeability edema and (5) Hsp90 inhibitors, which prevent and repair toxin-induced hyperpermeability. Unraveling the mechanism of action of these agents could contribute to the development of novel therapeutic strategies to combat permeability edema.

Indexed as

Acute Lung InjuryAdenosine TriphosphateChelating AgentsDrug Delivery SystemsEpitheliumHSP90 Heat-Shock ProteinsHumansPermeabilityPeroxisome Proliferator-Activated ReceptorsTumor Necrosis Factor-alphaAdenosine TriphosphateChelating AgentsHSP90 Heat-Shock ProteinsPeroxisome Proliferator-Activated ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID19428331
PMCPMC4474367
OpenAlexW1980611128

What OpenQuestion holds

Textmetadata
LicenceTDM
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.