作者: Silvana Balzan , Valter Lubrano
DOI: 10.1016/J.LFS.2018.02.024
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摘要: Abstract Altered production of reactive oxygen species (ROS), causing lipid peroxidation and DNA damage, contributes to the progression atherosclerosis cancer. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a lectin-like receptor for lipoproteins (ox-LDL) primarily expressed in endothelial cells vasculature-rich organs. LOX-1 receptors marker atherosclerosis, once activated by ox-LDL or other ligands, stimulates expression adhesion molecules, pro-inflammatory signaling pathways proangiogenic proteins, including NF-kB VEGF, vascular macrophages. Several different types cancer reported gene upregulation, numerous interplays exist concerning metabolic diseases One them involves NF-kB, an oncogenic protein that regulates transcription several inflammatory genes response. In model cellular transformation, MCF10A ER-Src, inhibition reduces activation hypoxia pathways, suggesting mechanistic connection between transformation atherosclerosis. The remodeling proteins MMP-2 MMP-9 have been found increased angiogenesis atherosclerotic plaque also human prostate cells. this review, we outlined role atherogenesis tumorigenesis as potential link these diseases, could represent promising strategy treatment tumors.