Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
INSERM-UMR1149, Centre de Recherche sur l'Inflammation, and Sorbonne Paris Cité, Laboratoire d'Excellence Inflamex, Faculté de Médecine, Site Xavier Bichat, Université Paris Diderot, Paris, France.
Curr Vasc Pharmacol. 2020;18(3):204-214. doi: 10.2174/1570161117666190206234046.
Under physiological conditions, peripheral arteries release endogenous vascular-protective and antithrombotic agents. Endothelial cells actively synthesize vasoactive mediators, which regulate vascular tone and platelet reactivity thus preventing thrombosis. Atherosclerosis disrupts homeostasis and favours thrombosis by triggering pro-thrombotic responses in the vessels, platelet activation, aggregation as well as vasoconstriction, phenomena that ultimately lead to symptomatic lumen restriction or complete occlusion. In the present review, we will discuss the homeostatic role of arterial vessels in releasing vascular-protective agents, such as nitric oxide and prostacyclin, the role of pro- and anti-thrombotic vascular receptors as well as the contribution of circulating platelets and coagulation factors in triggering the pro-thrombotic response(s). We will discuss the pathological consequences of disrupting the protective pathways in the arteries and the pharmacological interventions along these pathways.
在生理条件下，外周动脉会释放内源性血管保护和抗血栓形成剂。内皮细胞积极合成血管活性介质，调节血管张力和血小板反应性，从而防止血栓形成。动脉粥样硬化通过触发血管内的促血栓形成反应、血小板激活、聚集以及血管收缩来破坏内稳态并促进血栓形成，这些现象最终导致有症状的管腔狭窄或完全闭塞。在本综述中，我们将讨论动脉血管在释放血管保护剂（如一氧化氮和前列环素）方面的生理平衡作用，讨论促血栓形成和抗血栓形成血管受体的作用，以及循环血小板和凝血因子在触发促血栓形成反应方面的作用。我们还将讨论破坏动脉保护途径的病理后果，以及沿着这些途径的药理学干预措施。
