Evidence map›Paper›PMID 24482375›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2014

Arguing the case for the autotaxin-lysophosphatidic acid-lipid phosphate phosphatase 3-signaling nexus in the development and complications of atherosclerosis.

Susan S Smyth, Paul Mueller, Fanmuyi Yang, J Anthony Brandon, Andrew J Morris

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 69 citations in OpenAlex.

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  14. Coronary Artery Disease Risk-AssociatedArteriosclerosis, thrombosis, and vascular biology · 2019
    Article
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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

5 authors at 1 institution in 1 country.

Susan S SmythFrom the Veterans Affairs Medical Center, Cardiovascular Medicine Service, Lexington, KY (S.S.S., A.J.M.); and Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY (S.S.S., P.M., F.Y., J.A.B., A.J.M.).
Paul Mueller
Fanmuyi Yang
J Anthony Brandon
Andrew J Morris
Veterans Health Administration · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2012 to 2017
$13.7M
Kentucky Center for Clinical and Translational ScienceUL1TR000117 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$13.3M
THROMBOSPONDIN1 MEDIATES MACROPHAGE INFILTRATION INTO ADIPOSE TISSUE AND PROMOTEP20RR021954 · NCRR · UNIVERSITY OF KENTUCKY · PI ECKHARDT, ERIK · 2008 to 2011
$8.3M
Role of Lipid Phosphatases in Cholesterol and Triglyceride SynthesisR01GM050388 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI MORRIS, ANDREW J · 1994 to 2011
$2.7M
Lysolipid Signaling in Cardovascular DiseaseR01HL078663 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SMYTH, SUSAN S. · 2004 to 2013
$2.5M
Kentucky Center for Clinical and Translational ScienceTL1TR000115 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$518k
Regulation of adipose cells by autotaxin / lysophosphatidic acid signalingI01BX001014 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI SMYTH, SUSAN S. · 2011 to 2014
–
Association of a common variant of the PPAP2B gene with cardiovascular disease.I01BX001984 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI MORRIS, ANDREW J · 2013 to 2016
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BLRD VA I01 BX001014BLRD VA I01 BX001984NCATS NIH HHS TL1 TR000115NCATS NIH HHS TL1TR000115NCATS NIH HHS UL1 TR000117NCATS NIH HHS UL1TR000117NCRR NIH HHS P20 RR021954NCRR NIH HHS P20RR021954NHLBI NIH HHS R01 HL078663NHLBI NIH HHS R01HL078663NIGMS NIH HHS P20 GM103527NIGMS NIH HHS P20GM103527NIGMS NIH HHS R01 GM050388
6 · The paper itself

Abstract

The structurally simple glycero- and sphingo-phospholipids, lysophosphatidic acid (LPA) and sphingosine-1-phosphate, serve as important receptor-active mediators that influence blood and vascular cell function and are positioned to influence the events that contribute to the progression and complications of atherosclerosis. Growing evidence from preclinical animal models has implicated LPA, LPA receptors, and key enzymes involved in LPA metabolism in pathophysiologic events that may underlie atherosclerotic vascular disease. These observations are supported by genetic analysis in humans implicating a lipid phosphate phosphatase as a novel risk factor for coronary artery disease. In this review, we summarize current understanding of LPA production, metabolism, and signaling as may be relevant for atherosclerotic and other vascular disease.

Indexed as

Adipose TissueAnimalsApolipoproteins EAtherosclerosisCoronary Artery DiseaseGenetic Predisposition to DiseaseHumansLysophospholipase DLysophospholipidsMiceMice, KnockoutPhosphatidate PhosphatasePhosphoric Diester HydrolasesPlaque, AtheroscleroticRiskSphingosineApolipoproteins Elipid phosphate phosphataselysophosphatidic acidLysophospholipase DLysophospholipidsPhosphatidate PhosphatasePhosphoric Diester HydrolasesPLPP3 protein, humanPlpp3 protein, mouseSphingosinesphingosine 1-phosphateatherosclerosislipid phosphate phosphataselysophosphatidic acid

Identifiers

PMID24482375
PMCPMC3944085
OpenAlexW2149557213

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.