Evidence map›Paper›PMID 19563700›Full record

ReviewExpert reviews in molecular medicine2009

Molecular mechanisms of endothelial hyperpermeability: implications in inflammation.

Puneet Kumar, Qiang Shen, Christopher D Pivetti, Eugene S Lee, Mack H Wu, Sarah Y Yuan

Open access · bronzeAbstract readReview
In one paragraph

Review in Expert reviews in molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed
10.5field-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

190 citing papers in PubMed, 374 citations in OpenAlex.

  1. Comparative inhibition by bilastine and cetirizine of histamine-induced wheal and flare responses in humans.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011
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  12. Neutrophil Extracellular Traps Affect Human Inner Ear Vascular Permeability.International journal of molecular sciences · 2024
    Article
  13. Article
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  15. Article
  16. Ethanol Extract ofAdvances in pharmacological and pharmaceutical sciences · 2024
    Article
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  19. Review
  20. Review

130 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

6 authors at 1 institution in 1 country.

Puneet KumarDivision of Research, Department of Surgery, University of California at Davis School of Medicine, Sacramento, CA 95758, USA.
Qiang Shen
Christopher D Pivetti
Eugene S Lee
Mack H Wu
Sarah Y Yuan
University of California, Davis · US

Funding

Microvascular Barrier Dysfunction in Thermal TraumaR01HL070752 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 2002 to 2018
$4.7M
NEUTROPHIL DEPENDENT REGULATION OF VENULAR PERMEABILITYR01HL061507 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 1999 to 2011
$3.4M
PKC Isoenzymes Diabetic Microvascular HyperpermeabilityR01HL084542 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI YUAN, SARAH Y · 2006 to 2010
$1.9M
VEGF Regulation of Microvascular PermeabilityR01HL073324 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI WU, MACK H · 2004 to 2008
$1.6M
NHLBI NIH HHS HL61507NHLBI NIH HHS HL70752NHLBI NIH HHS HL73324NHLBI NIH HHS HL84542NHLBI NIH HHS R01 HL061507NHLBI NIH HHS R01 HL070752NHLBI NIH HHS R01 HL073324NHLBI NIH HHS R01 HL084542
6 · The paper itself

Abstract

Endothelial hyperpermeability is a significant problem in vascular inflammation associated with trauma, ischaemia-reperfusion injury, sepsis, adult respiratory distress syndrome, diabetes, thrombosis and cancer. An important mechanism underlying this process is increased paracellular leakage of plasma fluid and protein. Inflammatory stimuli such as histamine, thrombin, vascular endothelial growth factor and activated neutrophils can cause dissociation of cell-cell junctions between endothelial cells as well as cytoskeleton contraction, leading to a widened intercellular space that facilitates transendothelial flux. Such structural changes initiate with agonist-receptor binding, followed by activation of intracellular signalling molecules including calcium, protein kinase C, tyrosine kinases, myosin light chain kinase, and small Rho-GTPases; these kinases and GTPases then phosphorylate or alter the conformation of different subcellular components that control cell-cell adhesion, resulting in paracellular hypermeability. Targeting key signalling molecules that mediate endothelial-junction-cytoskeleton dissociation demonstrates a therapeutic potential to improve vascular barrier function during inflammatory injury.

Indexed as

AnimalsCapillary PermeabilityCytoskeletonEndothelium, VascularHumansInflammationIntercellular JunctionsModels, Biological

Identifiers

PMID19563700
PMCPMC2828491
OpenAlexW1992855266

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.