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10.1126/scitranslmed.aad6100

http://scihub22266oqcxt.onion/10.1126/scitranslmed.aad6100
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C4878149!4878149!27053774
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suck abstract from ncbi


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pmid27053774      Sci+Transl+Med 2016 ; 8 (333): 333ra50
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  • Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming #MMPMID27053774
  • Zimmer S; Grebe A; Bakke SS; Bode N; Halvorsen B; Ulas T; Skjelland M; De Nardo D; Labzin LI; Kerksiek A; Hempel C; Heneka MT; Hawxhurst V; Fitzgerald ML; Trebicka J; Gustafsson JÅ; Westerterp M; Tall AR; Wright SD; Espevik T; Schultze JL; Nickenig G; Lütjohann D; Latz E
  • Sci Transl Med 2016[Apr]; 8 (333): 333ra50 PMID27053774show ga
  • Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol levels. Despite ongoing advances in the prevention and treatment of atherosclerosis, cardiovascular disease remains the leading cause of death worldwide. Continuous retention of apolipoprotein B-containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Since cholesterol accumulation and deposition of cholesterol crystals (CCs) triggers a complex inflammatory response, we tested the efficacy of the cyclic oligosaccharide 2-hydroxypropyl-?-cyclodextrin (CD), a compound that increases cholesterol solubility, in preventing and reversing atherosclerosis. Here we show that CD treatment of murine atherosclerosis reduced atherosclerotic plaque size and CC load, and promoted plaque regression even with a continued cholesterol-rich diet. Mechanistically, CD increased oxysterol production in both macrophages and human atherosclerotic plaques, and promoted liver X receptor (LXR)-mediated transcriptional reprogramming to improve cholesterol efflux and exert anti-inflammatory effects. In vivo, this CD-mediated LXR agonism was required for the anti-atherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Since CD treatment in humans is safe and CD beneficially affects key mechanisms of atherogenesis, it may therefore be used clinically to prevent or treat human atherosclerosis.
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