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Association of ADAMTS7 gene polymorphism with cardiovascular survival in coronary artery disease

2016Journal article Open access
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dc.contributor.authorPereira, A.
dc.contributor.authorPalma dos Reis, R.
dc.contributor.authorRodrigues, R.
dc.contributor.authorSousa, A. C.
dc.contributor.authorGomes, S.
dc.contributor.authorBorges, S.
dc.contributor.authorOrnelas, I.
dc.contributor.authorFreitas, A. I.
dc.contributor.authorGuerra, G.
dc.contributor.authorHenriques, E.
dc.contributor.authorRodrigues, M.
dc.contributor.authorFreitas, S.
dc.contributor.authorFreitas, C.
dc.contributor.authorBrehm, A.
dc.contributor.authorPereira, D.
dc.contributor.authorMendonça, M. I.
dc.date.accessioned2020-11-13T15:17:06Z
dc.date.available2020-11-13T15:17:06Z
dc.date.issued2016
dc.description.abstractRecent genetic studies have revealed an association between polymorphisms at the ADAMTS7 gene locus and coronary artery disease (CAD) risk. Functional studies have shown that a CAD-associated polymorphism (rs3825807) affects ADAMTS7 maturation and vascular smooth muscular cell (VSMC) migration. Here, we tested whether ADAMTS7 (A/G) SNP is associated with cardiovascular (CV) survival in patients with established CAD. A cohort of 1,128 patients with angiographic proven CAD, who were followed up prospectively for a mean follow-up period of 63 (range 6-182) mo, were genotyped for rs3825807 A/G. Survival statistics (Cox regression) compared heterozygous (AG) and wild-type (AA) with the reference homozygous GG. Kaplan-Meier (K-M) survival curves were performed according to ADAMTS7 genotypes for CV mortality. Results showed that 47.3% of patients were heterozygous (AG), 36.5% were homozygous for the wild-type allele (AA) and only 16.2% were homozygous for the GG genotype. During the follow-up period, 109 (9.7%) patients died, 77 (6.8%) of CV causes. Survival analysis showed that AA genotype was an independent risk factor for CV mortality compared with reference genotype GG (HR = 2.7, P = 0.025). At the end of follow-up, the estimated survival probability (K-M) was 89.8% for GG genotype, 82.2% for AG and 72.3% for AA genotype (P = 0.039). Carriage of the mutant G allele of the ADAMTS7 gene was associated with improved CV survival in patients with documented CAD. The native overfunctional ADAMTS7 allele (A) may accelerate VSMC migration and lead to neointimal thickening, atherosclerosis progression and acute plaque events. ADAMTS7 gene should be further explored in CAD for risk prediction, mechanistic and therapeutic goals.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationPereira, A., Palma Dos Reis, R., Rodrigues, R., Sousa, A. C., Gomes, S., Borges, S., ... & Rodrigues, M. (2016). Association of ADAMTS7 gene polymorphism with cardiovascular survival in coronary artery disease. Physiological genomics, 48(11), 810-815.pt_PT
dc.identifier.doi10.1152/physiolgenomics.00059.2016pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.13/2979
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherAmerican Physiological Societypt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectADAMTS7 Proteinpt_PT
dc.subjectCoronary artery diseasept_PT
dc.subjectFemalept_PT
dc.subjectHumanspt_PT
dc.subjectMalept_PT
dc.subjectMiddle Agedpt_PT
dc.subjectPolymorphism, Single Nucleotidept_PT
dc.subjectSurvival Analysispt_PT
dc.subjectGenetic Association Studiespt_PT
dc.subjectGenetic Predisposition to Diseasept_PT
dc.subject.pt_PT
dc.subjectFaculdade de Ciências da Vidapt_PT
dc.titleAssociation of ADAMTS7 gene polymorphism with cardiovascular survival in coronary artery diseasept_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage815pt_PT
oaire.citation.startPage810pt_PT
oaire.citation.titlePhysiological Genomicspt_PT
oaire.citation.volume48(11)pt_PT
person.familyNameBrehm
person.givenNameAntonio
person.identifier.ciencia-id3613-8D1F-0EDF
person.identifier.orcid0000-0003-3168-5340
person.identifier.scopus-author-idAuthor ID 7006085833
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication62d279e2-247a-4652-a370-3e8c2a846e31
relation.isAuthorOfPublication.latestForDiscovery62d279e2-247a-4652-a370-3e8c2a846e31

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