Evidence map›Paper›PMID 29153655›Full record

ArticleThe American journal of pathology2017

Clinical Evidence Supports a Protective Role for CXCL5 in Coronary Artery Disease.

Saranya Ravi, Robert N Schuck, Eleanor Hilliard, Craig R Lee, Xuming Dai, Kaitlin Lenhart, Monte S Willis, Brian C Jensen, George A Stouffer, Cam Patterson and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2017. 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
0.8field-weighted citation impact, top 29% 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, 52 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Saranya RaviMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Robert N SchuckDivision of Pharmacotherapy and Experimental Therapeutics, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Eleanor HilliardMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Craig R LeeMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Division of Pharmacotherapy and Experimental Therapeutics, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Xuming DaiMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Eshelman School of Pharmacy, the Division of Cardiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Kaitlin LenhartMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Monte S WillisMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Department of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Brian C JensenMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Eshelman School of Pharmacy, the Division of Cardiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
George A StoufferMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Eshelman School of Pharmacy, the Division of Cardiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Cam PattersonPresbyterian Hospital/Weill-Cornell Medical Center, New York, New York.
Jonathan C SchislerMcAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Department of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. Electronic address: schisler@unc.edu.
University of North Carolina at Chapel Hill · USPresbyterian Hospital · US

Funding

Pre-doctoral Training Program in Integrative Vascular BiologyT32HL069768 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Christopher P. Mack · 2002 to 2026
$9.7M
Myocyte Signaling and the Response to StressR37HL065619 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PATTERSON, WINSTON C · 2010 to 2019
$3.7M
American Heart Association-American Stroke Association 11PRE7240059American Heart Association-American Stroke Association 16GRNT29300003NHLBI NIH HHS L30 HL104750NHLBI NIH HHS R37 HL065619NHLBI NIH HHS T32 HL069768
6 · The paper itself

Abstract

Our goal was to measure the association of CXCL5 and molecular phenotypes associated with coronary atherosclerosis severity in patients at least 65 years old. CXCL5 is classically defined as a proinflammatory chemokine, but its role in chronic inflammatory diseases, such as coronary atherosclerosis, is not well defined. We enrolled individuals who were at least 65 years old and undergoing diagnostic cardiac catheterization. Coronary artery disease (CAD) severity was quantified in each subject via coronary angiography by calculating a CAD score. Circulating CXCL5 levels were measured from plasma, and both DNA genotyping and mRNA expression levels in peripheral blood mononuclear cells were quantified via microarray gene chips. We observed a negative association of CXCL5 levels with CAD at an odds ratio (OR) of 0.46 (95% CI, 0.27-0.75). Controlling for covariates, including sex, statin use, hypertension, hyperlipidemia, obesity, self-reported race, smoking, and diabetes, the OR was not significantly affected [OR, 0.54 (95% CI, 0.31-0.96)], consistent with a protective role for CXCL5 in coronary atherosclerosis. We also identified 18 genomic regions with expression quantitative trait loci of genes correlated with both CAD severity and circulating CXCL5 levels. Our clinical findings are consistent with the emerging link between chemokines and atherosclerosis and suggest new therapeutic targets for CAD.

Indexed as

AgedChemokine CXCL5Coronary Artery DiseaseFemaleHumansMaleChemokine CXCL5CXCL5 protein, human

Identifiers

PMID29153655
PMCPMC5718092
OpenAlexW2769465037

What OpenQuestion holds

Textmetadata
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.