Evidence map›Paper›PMID 32541676›Full record

ArticleScientific reports2020

Omentin: a biomarker of cardiovascular risk in individuals with axial spondyloarthritis.

Fernanda Genre, Javier Rueda-Gotor, Sara Remuzgo-Martínez, Verónica Pulito-Cueto, Alfonso Corrales, Verónica Mijares, Leticia Lera-Gómez, Virginia Portilla, Rosa Expósito, Cristina Mata and 15 more

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Observational
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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

25 authors.

Fernanda Genre *Research group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Javier Rueda-Gotor *Research group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Sara Remuzgo-Martínez *Research group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Verónica Pulito-CuetoResearch group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Alfonso CorralesResearch group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Verónica MijaresResearch group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Leticia Lera-GómezResearch group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Virginia PortillaResearch group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Rosa ExpósitoRheumatology Division, Hospital Comarcal de Laredo, Laredo, Spain.
Cristina MataRheumatology Division, Hospital Comarcal de Laredo, Laredo, Spain.
Ricardo BlancoResearch group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain.
Javier LlorcaDepartment of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBERESP, IDIVAL, Santander, Spain.
Vanesa Hernández-HernándezRheumatology Division, Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain.
Esther VicenteRheumatology Division, Hospital Universitario de La Princesa, IIS-Princesa, Madrid, Spain.
Cristina Fernández-CarballidoRheumatology Division, Hospital Universitario de San Juan, Alicante, Spain.
María Paz Martínez-VidalRheumatology Division, Hospital General Universitario de Alicante, Alicante, Spain.
David Castro-CorredorRheumatology Division, Hospital General Universitario de Ciudad Real, Ciudad Real, Spain.
Joaquín Anino-FernándezRheumatology Division, Hospital General Universitario de Ciudad Real, Ciudad Real, Spain.
Carlos Rodríguez-LozanoRheumatology Division, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain.
Oreste GualilloSERGAS and IDIS, The NEIRID Group, Santiago University Clinical Hospital, Santiago de Compostela, Spain.ORCID http://orcid.org/0000-0002-7154-1328
Juan Carlos Quevedo-AbeledoRheumatology Division, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain.
Santos CastañedaRheumatology Division, Hospital Universitario de La Princesa, IIS-Princesa, Madrid, Spain.
Iván Ferraz-AmaroRheumatology Division, Hospital Universitario de Canarias, Santa Cruz de Tenerife, Spain.
Raquel López-MejíasResearch group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain. rlopezmejias78@gmail.com.ORCID http://orcid.org/0000-0003-0548-2689
Miguel Á González-GayResearch group on genetic epidemiology and atherosclerosis in systemic diseases and in metabolic diseases of the musculoskeletal system, IDIVAL, Santander, Spain. miguelaggay@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular (CV) disease is the main cause of mortality in axial spondyloarthritis (axSpA). CV risk is enhanced by dysregulation of adipokines. Low omentin levels were associated with metabolic dysfunction and CV disease in conditions different from axSpA. Accordingly, we evaluated the genetic and functional implication of omentin in CV risk and subclinical atherosclerosis in a cohort of 385 axSpA patients. Subclinical atherosclerosis was evaluated by carotid ultrasound. Omentin rs12409609, in linkage disequilibrium with a polymorphism associated with CV risk, was genotyped in 385 patients and 84 controls. Serum omentin levels were also determined. omentin mRNA expression was assessed in a subgroup of individuals. Serum and mRNA omentin levels were lower in axSpA compared to controls. Low serum omentin levels were related to male sex, obesity, inflammatory bowel disease (IBD) and high atherogenic index. rs12409609 minor allele was associated with low omentin mRNA expression in axSpA. No association was observed with subclinical atherosclerosis at the genetic or functional level. In conclusion, in our study low omentin serum levels were associated with CV risk factors in axSpA. Furthermore, rs12409609 minor allele may be downregulating the expression of omentin. These data support a role of omentin as a CV risk biomarker in axSpA.

Indexed as

AdultBiomarkersCardiovascular DiseasesCase-Control StudiesCytokinesFemaleGPI-Linked ProteinsHumansLectinsLinkage DisequilibriumMaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsSpondylarthritisBiomarkersCytokinesGPI-Linked ProteinsITLN1 protein, humanLectins

Identifiers

PMID32541676
PMCPMC7295748

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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.