Evidence map›Paper›PMID 24794532›Full record

ReviewCellular signalling2014

P21-activated kinase in inflammatory and cardiovascular disease.

Domenico M Taglieri, Masuko Ushio-Fukai, Michelle M Monasky

Abstract readReview
In one paragraph

Review in Cellular signalling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  13. Exploring the Pharmacological Mechanisms ofBioMed research international · 2021
    Article
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  19. Effects ofFrontiers in pharmacology · 2019
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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

3 authors at 2 institutions in 2 countries.

Domenico M TaglieriDepartment of Anesthesia and General Intensive Care Unit, Humanitas Research Hospital, Via Manzoni 56, Rozzano, 20089 (Milano), Italy. Electronic address: domenico.taglieri@humanitas.it.
Masuko Ushio-FukaiDepartment of Pharmacology, Center for Lung and Vascular Biology, Center for Cardiovascular Research, University of Illinois at Chicago, 835 S. Wolcott Ave. E403 MSB, M/C868, Chicago, IL 60612, USA. Electronic address: mfukai@uic.edu.
Michelle M MonaskyCardiovascular Research Center, Humanitas Research Hospital, Via Manzoni 113, Rozzano, 20089 (Milano), Italy. Electronic address: michelle.monasky@humanitasresearch.it.
IRCCS Humanitas Research Hospital · ITUniversity of Illinois Chicago · US

Funding

Copper transport protein and inflammatory angiogenesisR01HL116976 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FUKAI, TOHRU, USHIO-FUKAI, MASUKO · 2013 to 2016
$2.9M
Role of Cysteine Sulfenic Acid Formation in Compartmentalization of VEGF SignalinR21HL112293 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI USHIO-FUKAI, MASUKO · 2013 to 2014
$435k
NHLBI NIH HHS R01 HL116976NHLBI NIH HHS R01HL116976NHLBI NIH HHS R21 HL112293NHLBI NIH HHS R21HL112293
6 · The paper itself

Abstract

P-21 activated kinases, or PAKs, are serine-threonine kinases that serve a role in diverse biological functions and organ system diseases. Although PAK signaling has been the focus of many investigations, still our understanding of the role of PAK in inflammation is incomplete. This review consolidates what is known about PAK1 across several cell types, highlighting the role of PAK1 and PAK2 in inflammation in relation to NADPH oxidase activation. This review explores the physiological functions of PAK during inflammation, the role of PAK in several organ diseases with an emphasis on cardiovascular disease, and the PAK signaling pathway, including activators and targets of PAK. Also, we discuss PAK1 as a pharmacological anti-inflammatory target, explore the potentials and the limitations of the current pharmacological tools to regulate PAK1 activity during inflammation, and provide indications for future research. We conclude that a vast amount of evidence supports the idea that PAK is a central molecule in inflammatory signaling, thus making PAK1 itself a promising prospective pharmacological target.

Indexed as

Cardiovascular DiseasesHumansInflammationNADPH Oxidasesp21-Activated KinasesReceptor for Advanced Glycation End ProductsReceptor Protein-Tyrosine KinasesReceptors, ImmunologicSignal TransductionNADPH Oxidasesp21-Activated KinasesReceptor for Advanced Glycation End ProductsReceptor Protein-Tyrosine KinasesReceptors, ImmunologicCardiacCell migrationCytoskeletal dynamicsNADPH oxidasePAK1PAK2

Identifiers

PMID24794532
PMCPMC4129940
OpenAlexW2118552416

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.