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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, UNASSIGNED. Meshes: Animals, Aorta, Thoracic, Aortic Diseases, Apolipoproteins E, Atherosclerosis, Bone Marrow Transplantation, Cell Degranulation, Cells, Cultured, Cholesterol, Collagen, Diet, High-Fat, Disease Models, Animal, Disease Progression, Foam Cells, Genetic Predisposition to Disease, Macrophages, Peritoneal, Male, Mast Cells, Mice, Knockout, Muscle, Smooth, Vascular, Nicotine, Nicotinic Agonists, Nicotinic Antagonists, Phenotype, Plaque, Atherosclerotic, Proto-Oncogene Proteins c-kit, Signal Transduction, Time Factors, alpha7 Nicotinic Acetylcholine Receptor.
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Does nicotine accelerate Atherosclerosis in Apolipoprotein E-Deficient Mice by Activating α7 Nicotinic Acetylcholine Receptor on Mast Cells? Context: Cigarette smoking is an independent risk factor for atherosclerosis. Nicotine, the addictive component of cigarettes, induces mast cell (MC) release and contributes to atherogenesis. The purpose of this study was to determine whether nicotine accelerates atherosclerosis through MC-mediated mechanisms and whether MC stabilizer prevents this pathological process. Nicotine administration increased the size of atherosclerotic lesions in apolipoprotein E-deficient (Apoe
assistant
Activation of α7 nicotinic acetylcholine receptor on MCs is a mechanism by which nicotine enhances atherosclerosis. Final Decision: yes