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lüll Apolipoprotein A-I mimetic peptides Van Lenten BJ; Wagner AC; Anantharamaiah GM; Navab M; Reddy ST; Buga GM; Fogelman AMCurr Atheroscler Rep 2009[Jan]; 11 (1): 52-7Recent publications reveal the mechanism of action of apolipoprotein A-I (apoA-I) mimetic peptides to be the remarkable binding affinity that oxidized lipids have for these peptides compared with apoA-I. There was no difference in the binding affinity of oxidized lipids or in peptide efficacy in reducing inflammation and atherosclerosis in rabbits injected with peptides synthesized from all D- or all L-amino acids. The apoA-I mimetic peptide 4F increased the formation of pre-beta high-density lipoprotein, increased cholesterol efflux, and reduced lipoprotein oxidation in vitro; it increased antioxidants and vascular repair in type 1 diabetic rats; it improved vasodilation, oxidative stress, myocardial inflammation, and angiogenic potential in a mouse model of scleroderma; it reduced renal inflammation in low-density lipoprotein receptor-null mice fed a Western diet; it reduced arthritis in a rat model; it reduced adiposity, increased adiponectin levels, and improved insulin sensitivity in obese mice; and it improved high-density lipoprotein inflammatory properties in humans with coronary heart disease.|Animals[MESH]|Anti-Inflammatory Agents/pharmacology/therapeutic use[MESH]|Apolipoprotein A-I/*pharmacology/*therapeutic use[MESH]|Arthritis/drug therapy[MESH]|Atherosclerosis/prevention & control[MESH]|Cholesterol, HDL/blood[MESH]|Diabetes Mellitus/drug therapy[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|Hyperlipidemias/complications[MESH]|Nephritis/drug therapy/etiology[MESH]|Obesity/drug therapy[MESH]|Scleroderma, Systemic/drug therapy[MESH] |