Evidence map›Paper›PMID 22008516›Full record

ReviewMicrovascular research2012

Endothelial FAK as a therapeutic target in disease.

Giovanni A Infusino, Jeffrey R Jacobson

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 7% 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, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Study of the Active Components and Molecular Mechanism ofFrontiers in molecular biosciences · 2021
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Cortical Actin Dynamics in Endothelial Permeability.Current topics in membranes · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Neuronal Wiskott-Aldrich syndrome protein regulates TGF-β1-mediated lung vascular permeability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  15. Review
  16. Article
  17. Article
  18. Molecular pathways: not a simple tube--the many functions of blood vessels.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
    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

2 authors at 1 institution in 1 country.

Giovanni A InfusinoInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
Jeffrey R Jacobson
University of Illinois Chicago · US

Funding

Tissue Culture Biomechanical CoreP01HL058064 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GARCIA, JOE G. N. · 1998 to 2012
$27.8M
Integrin Beta 4 in Vascular Inflammatory ResponsesR01HL096887 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI JACOBSON, JEFFREY R · 2009 to 2013
$1.9M
NHLBI NIH HHS P01 HL058064NHLBI NIH HHS P01 HL 58064NHLBI NIH HHS R01 HL096887NHLBI NIH HHS R01 HL 96887
6 · The paper itself

Abstract

Focal adhesions (FA) are important mediators of endothelial cytoskeletal interactions with the extracellular matrix (ECM) via transmembrane receptors, integrins and integrin-associated intracellular proteins. This communication is essential for a variety of cell processes including EC barrier regulation and is mediated by the non-receptor protein tyrosine kinase, focal adhesion kinase (FAK). As FA mediate the basic response of EC to a variety of stimuli and FAK is essential to these responses, the idea of targeting EC FAK as a therapeutic strategy for an assortment of diseases is highly promising. In particular, inhibition of FAK could prove beneficial in a variety of cancers via effects on EC proliferation and angiogenesis, in acute lung injury (ALI) via the attenuation of lung vascular permeability, and in rheumatoid arthritis via reductions in synovial angiogenesis. In addition, there are potential therapeutic benefits of FAK inhibition in cardiovascular disease and diabetic nephropathy as well. Several drugs that target EC FAK are now in existence and include agents currently under investigation in preclinical models as well as drugs that are readily available such as the sphingolipid analog FTY720 and statins. As the role of EC FAK in the pathogenesis of a variety of diseases continues to be explored and new insights are revealed, drug targeting of FAK will continue to be an important area of investigation and may ultimately lead to highly novel and effective strategies to treat these diseases.

Indexed as

Acute Lung InjuryAngiogenesis InhibitorsAnimalsAntirheumatic AgentsArthritis, RheumatoidCardiovascular AgentsCardiovascular DiseasesDiabetic NephropathiesEndothelial CellsFocal Adhesion Protein-Tyrosine KinasesHumansNeoplasmsNeovascularization, PathologicProtein Kinase InhibitorsRespiratory System AgentsSignal TransductionAngiogenesis InhibitorsAntirheumatic AgentsCardiovascular AgentsFocal Adhesion Protein-Tyrosine KinasesProtein Kinase InhibitorsRespiratory System Agents

Identifiers

PMID22008516
PMCPMC3232342
OpenAlexW2007066267

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.