Evidence map›Paper›PMID 28449647›Full record

ArticleBMC medical genetics2017

PEAR1 is not a major susceptibility gene for cardiovascular disease in a Flemish population.

Wen-Yi Yang, Thibault Petit, Nicholas Cauwenberghs, Zhen-Yu Zhang, Chang-Sheng Sheng, Lutgarde Thijs, Erika Salvi, Benedetta Izzi, Christophe Vandenbriele, Fang-Fei Wei and 10 more

Open access · goldAbstract read
In one paragraph

Article in BMC medical genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 15 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

20 authors at 6 institutions in 3 countries.

Wen-Yi YangStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Thibault PetitStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Nicholas CauwenberghsStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Zhen-Yu ZhangStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Chang-Sheng ShengStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Lutgarde ThijsStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Erika SalviGenomics and Bioinformatics Platform at Filarete Foundation, Department of Health Sciences and Graduate School of Nephrology, Division of Nephrology, San Paolo Hospital, University of Milan, Milan, Italy.
Benedetta IzziDepartment of Cardiovascular Sciences, Centre for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium.
Christophe VandenbrieleDepartment of Cardiovascular Sciences, Centre for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium.
Fang-Fei WeiStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Yu-Mei GuStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Lotte JacobsStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Lorena CitterioDivision of Nephrology and Dialysis, IRCCS San Raffaele Scientific Institute, University Vita-Salute San Raffaele, Milan, Italy.
Simona Delli CarpiniDivision of Nephrology and Dialysis, IRCCS San Raffaele Scientific Institute, University Vita-Salute San Raffaele, Milan, Italy.
Cristina BarlassinaGenomics and Bioinformatics Platform at Filarete Foundation, Department of Health Sciences and Graduate School of Nephrology, Division of Nephrology, San Paolo Hospital, University of Milan, Milan, Italy.
Daniele CusiGenomics and Bioinformatics Platform at Filarete Foundation, Department of Health Sciences and Graduate School of Nephrology, Division of Nephrology, San Paolo Hospital, University of Milan, Milan, Italy.
Marc F HoylaertsDepartment of Cardiovascular Sciences, Centre for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium.
Peter VerhammeDepartment of Cardiovascular Sciences, Centre for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium.
Tatiana KuznetsovaStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium.
Jan A StaessenStudies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium. jan.staessen@med.kuleuven.be.
KU Leuven · BEFondazione Filarete · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITMaastricht University · NLUniversity of Milan · ITVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlatelet Endothelial Aggregation Receptor 1 (PEAR1), a membrane protein highly expressed in platelets and endothelial cells, plays a role in platelet contact-induced activation, sustained platelet aggregation and endothelial function. Previous reports implicate PEAR1 rs12041331 as a variant influencing risk in patients with coronary heart disease. We investigated whether genetic variation in PEAR1 predicts cardiovascular outcome in a white population.

methodsIn 1938 participants enrolled in the Flemish Study on Environment, Genes and Health Outcomes (51.3% women; mean age 43.6 years), we genotyped 9 tagging SNPs in PEAR1, measured baseline cardiovascular risk factors, and recorded Cardiovascular disease incidence. For SNPs, we contrasted cardiovascular disease incidence of minor-allele heterozygotes and homozygotes (variant) vs. major-allele homozygotes (reference) and for haplotypes carriers vs. non-carriers. In adjusted analyses, we accounted for family clusters and baseline covariables, including sex, age, body mass index, mean arterial pressure, the total-to-HDL cholesterol ratio, smoking and drinking, antihypertensive drug treatment, and history of cardiovascular disease and diabetes mellitus.

resultsOver a median follow-up of 15.3 years, 238 died and 181 experienced a major cardiovascular endpoint. The multivariable-adjusted hazard ratios of eight PEAR1 SNPs, including rs12566888, ranged from 0.87 to 1.07 (P ≥0.35) and from 0.78 to 1.30 (P ≥0.15), respectively. The hazard ratios of three haplotypes with frequency ≥10% ranged from 0.93 to 1.11 (P ≥0.49) for mortality and from 0.84 to 1.03 (P ≥0.29) for a cardiovascular complications. These results were not influenced by intake of antiplatelet drugs, nonsteroidal anti-inflammatory drugs, or both (P-values for interaction ≥ 0.056).

conclusionsIn a White population, we could not replicate previous reports from experimental studies or obtained in patients suggesting that PEAR1 might be a susceptibility gene for cardiovascular complications.

Indexed as

Genetic Predisposition to DiseaseAdultBelgiumCardiovascular DiseasesFemaleHaplotypesHumansMaleMiddle AgedPolymorphism, Single NucleotideReceptors, Cell SurfacePEAR1 protein, humanReceptors, Cell SurfaceCardiovascular riskClinical geneticsPEAR1Population scienceReplication research

Identifiers

PMID28449647
PMCPMC5408434
OpenAlexW2609660873

What OpenQuestion holds

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Registered trials

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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.