Stromal cell-derived factor-1-30A polymorphism is associated with decreased risk of myocardial infarction and early endothelial disturbance (Articolo in rivista)

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  • Stromal cell-derived factor-1-30A polymorphism is associated with decreased risk of myocardial infarction and early endothelial disturbance (Articolo in rivista) (literal)
Anno
  • 2014-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.2459/JCM.0000000000000068 (literal)
Alternative label
  • Andrea Borghini, Silverio Sbrana, Cecilia Vecoli, Antonella Mercuri, Stefano Turchi, Clara Carpeggiani, Antonio L'Abbate and Maria G. Andreassi (2014)
    Stromal cell-derived factor-1-30A polymorphism is associated with decreased risk of myocardial infarction and early endothelial disturbance
    in Journal of cardiovascular medicine (Hagerstown, Md. : Online)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Andrea Borghini, Silverio Sbrana, Cecilia Vecoli, Antonella Mercuri, Stefano Turchi, Clara Carpeggiani, Antonio L'Abbate and Maria G. Andreassi (literal)
Pagina inizio
  • 710 (literal)
Pagina fine
  • 716 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 15 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 7 (literal)
Note
  • PubMed (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Institute of Clinical Physiology, CNR, via Moruzzi 1, 56124 Pisa, Italy (literal)
Titolo
  • Stromal cell-derived factor-1-30A polymorphism is associated with decreased risk of myocardial infarction and early endothelial disturbance (literal)
Abstract
  • Aim: Genome-wide association studies have identified single-nucleotide polymorphisms at the 10q11 locus as risk factors for myocardial infarction (MI). This locus lies upstream (?80 kb) of the stromal cell-derived factor-1 (SDF1) gene that codes for a chemokine with protective atherogenetic effects and with a major role in the mobilization, homing, and differentiation of endothelial progenitor cells (EPCs). The purpose of this study was to investigate the possible association of SDF1-3'A polymorphism, that upregulates SDF1 protein expression, with MI as well as early endothelial dysfunction and atherosclerosis in young healthy subjects. Methods: 200 patients (181 men age 57.3+/-7.7 years) and 230 healthy controls (96 men, age 52+/-11.9 years) were recruited to investigate the association between MI and SDF1-30A polymorphism. The relationship between SDF1-3'A polymorphism, brachial artery flow-mediated dilation, and the number of circulating EPCs was examined in 50 healthy young adults. Results: A significant difference in SDF1-3'A genotype distribution was observed between patients and controls (P=0.006). Patients carrying the A allele had a significantly reduced MI risk compared with subjects with GG genotype (odds ratio=0.5, 95% CI=0.3-0.9, P=0.001). SDF1-3'A polymorphism presented a significant interaction with other cardiovascular risk factors (Pinteraction<0. 0001). Controls carrying the A allele showed significantly higher flow-mediated dilation (13.9+/-4.9 vs 10.8+/-4.3, P=0.03) and significantly higher values of EPCs (0.029+/-0.009 vs 0.022+/-0.008, P=0.02) compared with GG homozygotes. Conclusion: SDF1-3'A polymorphism is associated with a decreased risk of MI and early endothelial dysfunction, strongly confirming the important atherogenic role of the SDF1 gene at the clinical level. (literal)
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