Lowery Curtis Lee, Woulfe Donna, Kilic Fusun
Departments of Biochemistry and Molecular Biology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, United States.
Department of Biological Sciences, University of Delaware, Newark, DE, United States.
Front Neurosci. 2019 Mar 4;13:32. doi: 10.3389/fnins.2019.00032. eCollection 2019.
Cigarette smoking is one of the major causes of coronary heart disease with a thirty percent mortality rate in the United States. Cigarette smoking acting on the central nervous system (CNS) to stimulate the sympathetic nervous system (SNS) through, which facilitates the secretion of serotonin (5-HT) and catecholamines to supraphysiological levels in blood. The enhanced levels of 5-HT and catecholamines in smokers' blood are associated with increases in G protein-coupled receptor signaling and serotonylation of small GTPases, which in turn lead to remodeling of cytoskeletal elements to enhance granule secretion and promote unique expression of sialylated -glycan structures on smokers' platelets. These mechanisms enhance aggregation and adhesion of smokers' platelets relative to those of non-smokers. This review focuses on the known mechanisms by which 5-HT and SERT, in coordinated signaling with catecholamines, impacts cigarette smokers' platelet biology.
在美国,吸烟是冠心病的主要病因之一,其死亡率达30%。吸烟作用于中枢神经系统(CNS),通过刺激交感神经系统(SNS),促使血清素(5-HT)和儿茶酚胺分泌至血液中的超生理水平。吸烟者血液中5-HT和儿茶酚胺水平的升高与G蛋白偶联受体信号增强及小GTP酶的血清素化有关,这反过来会导致细胞骨架成分重塑,以增强颗粒分泌,并促进吸烟者血小板上唾液酸化聚糖结构的独特表达。相对于不吸烟者,这些机制增强了吸烟者血小板的聚集和黏附。本综述聚焦于5-HT和5-羟色胺转运体(SERT)与儿茶酚胺协同信号传导影响吸烟者血小板生物学的已知机制。