%0 Journal Article
%T Soluble Lectin-Like Oxidized Low Density Lipoprotein Receptor-1 as a Biochemical Marker for Atherosclerosis-Related Diseases
%A Angela Pirillo
%A Alberico Luigi Catapano
%J Disease Markers
%D 2013
%R 10.1155/2013/716325
%X Lectin-like oxidized low density lipoprotein receptor-1 (LOX-1), the main oxidized low-density lipoprotein (OxLDL) in endothelial cells, is upregulated in atherosclerotic lesions and is involved in several cellular processes that regulate the pathogenesis of atherosclerosis. The LOX-1 expressed on the cell surface can be proteolytically cleaved and released in a soluble form (sLOX-1) in the circulation under pathological conditions. Serum levels of sLOX-1, in fact, are elevated at the early stages of acute coronary syndrome and are associated with coronary plaque vulnerability and with the presence of multiple complex coronary lesions. Moreover, in subjects with stable CAD, levels of serum sLOX-1 are associated with the presence of lesions in the proximal and mid-segments of the left anterior descending artery that are the most prone to rupture; in subjects undergoing percutaneous coronary intervention, baseline preprocedural serum sLOX-1 levels are associated with the incidence of periprocedural myocardial infarction. Altogether, these findings suggest that circulating levels of sLOX-1 might be a diagnostic and prognostic marker for atherosclerotic-related events. 1. Introduction High levels of low density lipoprotein (LDL) represent a major risk factor for atherosclerosis, since the oxidation of LDL is a key process in the initiation and progression of atherosclerotic lesion development. Oxidized LDL (OxLDL) acts through the interaction with several scavenger receptors, expressed differentially on the surface of the cells of the arterial wall and inflammatory circulating cells involved in the atherosclerotic process. Among these receptors, lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) has been identified as the main endothelial receptor for OxLDL [1]; however, also macrophages and smooth muscle cells (SMCs) express LOX-1 [2]. Several proinflammatory stimuli, including tumor necrosis factor (TNF ), C-reactive protein (CRP), interleukin-1 (IL-1), angiotensin II, and endothelin-1, and proatherogenic conditions (dyslipidemia, diabetes, hypertension) increase LOX-1 expression [3]. Through the interaction with LOX-1, OxLDL activates endothelial cells and induces endothelial dysfunction, SMC proliferation, and apoptosis; participates in the transformation of macrophages into foam cells, and induces platelet activation [3]. LOX-1 is undetectable in healthy vessels but overexpressed in atherosclerotic lesions [2], where it actively participates in the initiation and progression of the disease, as demonstrated by LOX-1 deletion or
%U http://www.hindawi.com/journals/dm/2013/716325/