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  • Association of single nucleotide polymorphisms in the oxidised LDL receptor 1 (OLR1) gene in patients with acute myocardial infarction

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Association of single nucleotide polymorphisms in the oxidised LDL receptor 1 (OLR1) gene in patients with acute myocardial infarction
  1. R Mango1,
  2. F Clementi1,
  3. P Borgiani1,
  4. G B Forleo1,
  5. M Federici1,
  6. G Contino1,
  7. E Giardina1,
  8. L Garza2,
  9. I E Fahdi2,
  10. R Lauro1,
  11. J L Mehta2,
  12. G Novelli1,
  13. F Romeo1
  1. 1Centre of Excellence for Genomic Risk Assessment in Multifactorial and Complex Diseases, School of Medicine, Tor Vergata University of Rome, Italy
  2. 2Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, USA
  1. Correspondence to:
 Giuseppe Novelli
 Dipartimento di Biopatologia e Diagnostica per Immagini, Università di Roma “Tor Vergata”, Via Montpellier 1 00133 Roma, Italy; novellimed.uniroma2.it

https://doi.org/10.1136/jmg.40.12.933

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    Acute myocardial infarction (AMI) is a significant cause of mortality and morbidity. Substantial data support a plausible role for oxidised LDL (oxLDL) in the aetiology of this disease.1,2 The human OLR1 (or LOX 1) gene encodes the endothelium derived lectin-like oxidised low density lipoprotein (oxLDL) receptor, which is involved in the binding, internalisation, and proteolytic degradation of oxLDL, suggesting that it may play a significant role in atherogenesis.3 OLR1 is considered a good candidate for atherosclerosis and AMI since it is induced in vitro by inflammatory cytokines and in vivo by pro-atherogenic conditions like hypertension, hyperlipidaemia, and diabetes mellitus.4 Recently, upregulation of OLR1 has been shown in ischaemia reperfusion injury in the rat.5 OLR1 acts as a mediator of “endothelial dysfunction” favouring superoxide generation, inhibiting nitric oxide production, and enhancing endothelial adhesiveness for monocytes.6–8 It is noteworthy that the versatile activities of OLR1 also include the ability to bind not only oxLDL, but also aged red blood cells, apoptotic cells, and activated platelets.4 With this background, we sought to validate the hypothesis of OLR1 involvement in atherosclerosis and AMI by defining OLR1 genetic variation by an association study of intragenic SNPs.

    METHODS

    Study subjects

    The study included 150 individuals with AMI who were referred to the Centre of Atherosclerosis at the Medical School of the Tor Vergata University of Rome. All cases were clinically evaluated and all underwent coronary angiography and left ventriculography. The diagnosis of AMI was based on typical electrocardiographic changes and increased serum activities of at least two enzymes, such as creatine kinase, aspartate aminotransferase, and lactate dehydrogenase. The diagnosis was confirmed by the presence of wall motion abnormality on left ventriculography and attendant stenosis (>50%) in any of the major coronary arteries or in the left main coronary artery on coronary …

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    Footnotes

    • This work was supported by grants from the Italian Ministry of Education, University and Research (Fondi Centri di Eccellenza 2000 and COFIN 2002).