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Health See other Health Articles Title: Creating A Medical Nanobot - Nanobots Block Macrophage-created Arterial Cholesterol Plaques in vivo Medicine's Fantastic Voyage Dear Colleagues, one goal for the clinical application of complex nanobots is to remove the cholesterol molecules from the arterial endothelium. These complex nanobots would eliminate atherosclerosis, but their creation is in the future. The research of Lewis, et al., however, may provide a much more rapid solution for eliminating arterial cholesterol (lipid-rich) plaques, atherosclerosis, heart attacks, strokes, and peripheral arterial occlusion. Their research cleverly used a simple nanobot to inhibit the cholesterol and lipid uptake by endothelial-associated macrophages. The macrophage uptake of lipids leads to the creation of arterial intimal fatty streaks, the precursors of lipid-rich atherosclerotic plaques. The plaques narrow the artery and quite often rupture. The ruptured plaque occludes the blood flow and/or produces downstream emboli. This occlusive/embolic event causes organ ischemia, namely heart attacks, central nervous system strokes, and peripheral extremity infarcts, depending upon the involved artery. Lewis DR, Peterson LK, York AW, et al., Sugar-based Amphiphilic Nanoparticles Arrest Atherosclerosis in vivo, Proc Nat Acad Sci, 2015;112:2693-2698. Elvin Price provides a summary of the work. Price E., iHeart nano: A Sweet Cure, Sci Transl Med - 2015;7:278ec40. 3/11/15 The gist: Sugar-based amphiphilic core-shell layered nanobots reduced atherogenesis in vivo by inhibiting the arterial macrophages' ability to ingest oxidized lipids. The inhibited ingestion of oxidized lipids by the macrophages reduced the activation of the scavenger receptor expression pathway within the macrophages. This process reduced plaque formation. Sugar-based amphiphilic macromolecules (AMs) were designed to competitively block the oxidized lipid uptake by the scavenger receptors on macrophages. The AMs were fabricated into serum-stable core/shell nanoparticles (NPs). These nanobots rapidly associated with the macrophages in the lipid-rich arterial plaques after intravenous injection. The nanobots inhibited disease progression (atherogenesis) in vivo by blocking the uptake of oxidized lipids. A library of AMs was designed and fabricated into nanoparticle (nanobot) compositions. These nanoparticles showed high binding and down-regulation (reduced production of the receptors within the macrophage) of both macrophage MSR1 and CD36 scavenger receptors. When these two receptors were blocked, minimal accumulation of oxidized lipids occurred in the macrophages. A mouse model of cardiovascular disease was used for the in vivo study (Apoe-/- mice) . When the nanobots were injected intravenously, confocal microscopy demonstrated the specific association of the nanobots with the lipid-rich arterial plaques, as compared with control nanoparticles. Within the plaques the nanobots inhibited the macrophage uptake of oxidized lipids. As compared to the control animals, the uptake inhibition produced a significant reduction in neointimal hyperplasia, lipid burden, cholesterol clefts, inflammation, and an overall 37% reduction in plaque occlusion. In other words, the atherogenic process was inhibited. The investigators concluded that scavenger receptor-targeted nanobots can shift macrophages to a less inflammatory state and are an effective approach to preventing atherogenesis. I agree that this is a very promising platform. Further development will be forthcoming. Potential nanotoxicity, as usual, must be adequately evaluated. Post Comment Private Reply Ignore Thread
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