Evidence map›Paper›PMID 23559624›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2013

Chemerin connects fat to arterial contraction.

Stephanie W Watts, Anne M Dorrance, Mark E Penfold, Jillian L Rourke, Christopher J Sinal, Bridget Seitz, Timothy J Sullivan, Trevor T Charvat, Janice M Thompson, Robert Burnett and 1 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
12.2field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
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  3. Chemerin/ChemerinR1 axis and inflammation-related diseases.Frontiers in molecular biosciences · 2026
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  14. Chemerin is resident to vascular tunicas and contributes to vascular tone.American journal of physiology. Heart and circulatory physiology · 2023
    Article
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27 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Stephanie W WattsDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824-1317, USA. wattss@msu.edu
Anne M Dorrance
Mark E Penfold
Jillian L Rourke
Christopher J Sinal
Bridget Seitz
Timothy J Sullivan
Trevor T Charvat
Janice M Thompson
Robert Burnett
Gregory D Fink
ChemoCentryx (United States) · US

Funding

SIGNALING MECHANISMS IN ARTERIES AND VEINS IN HYPERTENSIONP01HL070687 · NHLBI · MICHIGAN STATE UNIVERSITY · PI WATTS, STEPHANIE W · 2003 to 2019
$22.8M
NHLBI NIH HHS P01 HL070687NHLBI NIH HHS P01HL70687
6 · The paper itself

Abstract

objectiveObesity and hypertension are comorbid in epidemic proportion, yet their biological connection is largely a mystery. The peptide chemerin is a candidate for connecting fat deposits around the blood vessel (perivascular adipose tissue) to arterial contraction. We presently tested the hypothesis that chemerin is expressed in perivascular adipose tissue and is vasoactive, supporting the existence of a chemerin axis in the vasculature. APPROACH AND

resultsReal-time polymerase chain reaction, immunohistochemistry, and Western analyses supported the synthesis and expression of chemerin in perivascular adipose tissue, whereas the primary chemerin receptor ChemR23 was expressed both in the tunica media and endothelial layer. The ChemR23 agonist chemerin-9 caused receptor, concentration-dependent contraction in the isolated rat thoracic aorta, superior mesenteric artery, and mesenteric resistance artery, and contraction was significantly amplified (more than 100%) when nitric oxide synthase was inhibited and the endothelial cell mechanically removed or tone was placed on the arteries. The novel ChemR23 antagonist CCX832 inhibited phenylephrine-induced and prostaglandin F2α-induced contraction (+perivascular adipose tissue), suggesting that endogenous chemerin contributes to contraction. Arteries from animals with dysfunctional endothelium (obese or hypertensive) demonstrated a pronounced contraction to chemerin-9. Finally, mesenteric arteries from obese humans demonstrate amplified contraction to chemerin-9.

conclusionsThese data support a new role for chemerin as an endogenous vasoconstrictor that operates through a receptor typically attributed to function only in immune cells.

Indexed as

AdipokinesAdipose TissueAngiotensin IIAnimalsAorta, ThoracicBlotting, WesternChemokinesDisease Models, AnimalGene Expression RegulationHumansHypertensionImmunochemistryIntercellular Signaling Peptides and ProteinsMesenteric ArteriesMuscle, Smooth, VascularObesityAdipokinesAngiotensin IIChemokinesIntercellular Signaling Peptides and ProteinsPhenylephrineRARRES2 protein, humanRarres2 protein, ratadipose tissuechemerinChemR23PVATvasoconstriction

Identifiers

PMID23559624
PMCPMC3752465
OpenAlexW2136980622

What OpenQuestion holds

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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.