Crystal Lester 2006
Karina Nikogosian 2007
Ruja Shrestha 2007
Courtney Tucker 2007
atherosclerosis, reducing foam cell formation
Atherosclerosis is a cardiovascular inflammatory disease that occurs in major arteries and leads to heart attacks, stroke, and peripheral artery disease. This disease has a high mortality rate in Europe, the United States, and much of Asia. Researchers have developed a strain of genetically modified mice deficient in ApoE as a model for antherosclerosis. In this review, we aim to discuss the current advances at the molecular level and therapeutic approaches in the treatment of atherosclerosis. Two different secretory phospholipase A2’s (sPLA2), Groups V andX, hydrolyze low density lipoproteins(LDL) promoting spontaneous aggregation and generation of lyso-PC that evokes proatherogenic cellular events, respectively. The modified LDLs are internalized by the monocyte-derived macrophages via two scavenger receptor family members SR-A and CD36. Active macrophages induce the uptake of native LDL resulting in macrophage cholesterol accumulation, referred to as foam cell formation. Pathways that promote foam cell formation include lipoprotein lipase expressed in macrophages, chemokines such as MCP-1 expressed in monocytes, and fractalkine expressed on activated endothelial cells. Researchers have discovered that fractalkine, which undergoes ectodomain shedding by metalloproteinases, engages G-protein coupled receptors and upregulates integrins. Moreover, a single amino acid polymorphism of fractalkine receptors reduces coronary artery disease in vivo. There is currently no cure for atherosclerosis, but several studies have shown ways to treat the disease by reducing foam cell formation. These methods include immunization of immunoglobulin and LDL, anti MCP-1 gene therapy, and the use of the anti-oxidative effects of pomegranate juice.
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