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Identification, regulation and function of a novel lectin-like oxidized low-density lipoprotein receptor

^* Division of Cardiovascular Medicine, Department of Internal Medicine, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA

View larger version (44K): [in a new window]   Figure 1 Oxidized low-density lipoprotein (ox-LDL), tumor necrosis factor-alpha (TNF-), shear stress, reactive oxygen species (ROS), endothelin and angiotensin II (Ang II) increase the expression of lectin-like oxidized low-density lipoprotein receptor (LOX-1), which activates mitogen-activated protein kinases (MAPKs) and protein kinases (PKs), leading to activation of the transcription factor nuclear factor-B (NF-B). These steps play a crucial role in subsequent cell injury, through release of ROS and a reduction in endothelial nitric oxide synthase (eNOS). Enhanced activity of monocyte chemoattractant protein-1 (MCP-1) leads to expression of adhesion molecules. Simultaneously, LOX-1 activation leads to endothelial dysfunction, apoptosis and injury. These steps are collectively involved in atherogenesis. Along with decreases in eNOS, changes in Fas and bad lead to apoptosis. AT1 = angiotensin II type 1.