Mechanisms through which major risk factors accelerate diabetic angiopathy include low density lipoprotein (LDL) oxidation and advanced glycation end products (AGEs) formation. Lectin-like oxidized LDL receptor (LOX-1) is a newly identified vascular receptor for oxidized LDL (oxLDL) and AGEs. LOX-1 is up-regulated in vascular endothelium of diabetic animals and thus may be relevant to the development and progression of human diabetic vasculopathy. The mechanisms responsible for LOX-1 induction in diabetes remain unclear but appear to involve metabolic and inflammatory stimuli relevant to diabetes. Such factors may impact on LOX-1-mediated pro-atherogenic events, including endothelial dysfunction and plaque destabilization. Previous studies have shown that drugs commonly used in the treatment of type 2 diabetic patients, including statins and antidiabetic agents, inhibit endothelial LOX-1 expression. This review summarizes recent advances related to the role of LOX-1 in macrovascular diseases, its regulation by some derangements commonly found in diabetic patients and its modulation by vasculoprotective drugs.
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