Evidence map›Paper›PMID 21925517›Full record

ReviewMicrovascular research2012

Role of FAK in S1P-regulated endothelial permeability.

Patrick Belvitch, Steven M Dudek

Abstract readReview
In one paragraph

Review in Microvascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Post-translational modifications of S1PR1 and endothelial barrier regulation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Review
  7. Review
  8. Matrix stiffness regulates vascular integrity through focal adhesion kinase activity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  9. Article
  10. Cortical Actin Dynamics in Endothelial Permeability.Current topics in membranes · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Disorders of Vascular Permeability.Annual review of pathology · 2016
    Review
  16. Article
  17. Article
  18. Role of N-WASP in Endothelial Monolayer Formation and Integrity.The Journal of biological chemistry · 2015
    Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Patrick BelvitchInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
Steven M Dudek
University of Illinois Chicago · US

Funding

Tissue Culture Biomechanical CoreP01HL058064 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAL, RATNESHWAR · 1998 to 2012
$27.8M
Cortactin in Regulation of Pulmonary Vascular PermeabilityR01HL088144 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEK, STEVEN M · 2007 to 2011
$1.9M
NHLBI NIH HHS P01 HL058064NHLBI NIH HHS P01 HL 58064NHLBI NIH HHS R01 HL088144NHLBI NIH HHS R01 HL 88144
6 · The paper itself

Abstract

The vascular endothelium serves as a semi-selective barrier between the circulating contents of the blood and the tissues through which they flow. Disruption of this barrier results in significant organ dysfunction during devastating inflammatory syndromes such as sepsis and acute lung injury (ALI). Sphingosine 1-phosphate (S1P) is an endogenous lipid regulator of endothelial permeability that produces potent barrier enhancement via actin and junctional protein rearrangement and resultant cytoskeletal changes. A key effector protein in this S1P response is focal adhesion kinase (FAK), a highly conserved cytoplasmic tyrosine kinase involved in the engagement of integrins and assembly of focal adhesions (FA) through the catalysis of multiple downstream signals. After stimulation by S1P, endothelial FAK undergoes specific tyrosine phosphorylation that results in activation of the kinase and dynamic interactions with other effector molecules to improve the endothelial barrier. FAK participates in peripheral actin cytoskeletal rearrangement as well as cell-matrix (FA) and cell-cell (adherens junction) junctional complex strengthening that combine to decrease vascular permeability. This review summarizes the current knowledge of the role of FAK in mediating enhanced endothelial barrier function by S1P.

Indexed as

Capillary PermeabilityAnimalsEndothelial CellsEnzyme ActivationFocal Adhesion Protein-Tyrosine KinasesFocal AdhesionsHumansLysophospholipidsPhosphorylationSignal TransductionSphingosineFocal Adhesion Protein-Tyrosine KinasesLysophospholipidsSphingosinesphingosine 1-phosphate

Identifiers

PMID21925517
PMCPMC3684237
OpenAlexW2065061638

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.