© 2003 BMJ Publishing Group Ltd
LETTER TO JMG
Association of single nucleotide polymorphisms in the oxidised LDL receptor 1 (OLR1) gene in patients with acute myocardial infarction
1 Centre of Excellence for Genomic Risk Assessment in Multifactorial and Complex Diseases, School of Medicine, Tor Vergata University of Rome, Italy
2 Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, USA
Correspondence to:
Correspondence to:
Giuseppe Novelli
Dipartimento di Biopatologia e Diagnostica per Immagini, Università di Roma "Tor Vergata", Via Montpellier 1 00133 Roma, Italy; novelli@med.uniroma2.it
Keywords: denaturing high performance liquid chromatography; myocardial infarction; OLR1/LOX 1; SNPs
Abbreviations: AMI, acute myocardial infarction; CAD, coronary artery disease; OLR1, oxidised LDL receptor 1; OR, odds ratio; oxLDL, oxidised LDL; SNP, single nucleotide polymorphism; TNF, tumour necrosis factor
| The first 150 words of the full text of this article appear below. |
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.68 It is noteworthy that the versatile activities of OLR1 also include the ability to bind not
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