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

A cute 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. 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. 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. Recently, upregulation of OLR1 has been shown in ischaemia reperfusion injury in the rat. OLR1 acts as a mediator of ‘‘endothelial dysfunction’’ favouring superoxide generation, inhibiting nitric oxide production, and enhancing endothelial adhesiveness for monocytes. 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. 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.