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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.
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