血小板稳态
中文名称
通路描述
在正常条件下，血管内皮支持血管舒张，抑制血小板粘附和激活，抑制凝血，促进纤维蛋白降解，并具有抗炎特性。在急性血管创伤下，收缩机制占主导，内皮变为促凝血、促凝血和促炎性质。这是通过减少内皮舒张因子（腺苷、NO 和前列环素）来实现的，以及通过 ADP、血清素和血栓素对血管平滑肌细胞直接作用以引起收缩（Becker 等，2000）。环氧化酶 -2（COX-2）和内皮一氧化氮合酶（eNOS）主要在内皮细胞中表达。两者都是血管功能的重要调节因子。在正常条件下，层流诱导内皮细胞表达 COX-2 并合成前列环素（PGI2），后者进而刺激内皮一氧化氮合酶（eNOS）活性。PGI2 和 NO 均抑制血小板激活和聚集，CD39 外源性 ADP 酶也通过代谢血小板释放的 ADP 来抑制血小板激活和招募。
英文描述
Platelet homeostasis Under normal conditions the vascular endothelium supports vasodilation, inhibits platelet adhesion and activation, suppresses coagulation, enhances fibrin cleavage and is anti-inflammatory in character. Under acute vascular trauma, vasoconstrictor mechanisms predominate and the endothelium becomes prothrombotic, procoagulatory and proinflammatory in nature. This is achieved by a reduction of endothelial dilating agents: adenosine, NO and prostacyclin; and by the direct action of ADP, serotonin and thromboxane on vascular smooth muscle cells to elicit their contraction (Becker et al. 2000). Cyclooxygenase-2 (COX-2) and endothelial nitric oxide synthase (eNOS) are primarily expressed in endothelial cells. Both are important regulators of vascular function. Under normal conditions, laminar flow induces vascular endothelial COX-2 expression and synthesis of Prostacyclin (PGI2) which in turn stimulates endothelial Nitric Oxide Synthase (eNOS) activity. PGI2 and NO both oppose platelet activation and aggregation, as does the CD39 ecto-ADPase, which decreases platelet activation and recruitment by metabolizing platelet-released ADP.
所含基因
8 个基因