Tumor necrosis factor-α as trigger of platelet activation in patients with heart failure
Tumor necrosis factor-α as trigger of platelet activation in patients with heart failure
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DOI：
10.1182/blood-2005-03-1247
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发表时间：
2005-09-15
期刊：
影响因子：
20.3
通讯作者：
Violi, F
中科院分区：
文献类型：
--
作者：
Pignatelli, P;De Biase, L;Violi, F
心力衰竭（HF）患者的临床病史伴有动脉血栓栓塞。在该人群中报告了血小板活化，但其潜在机制尚未阐明。根据纽约心脏协会（NYHA）分级，42例HF患者的胶原诱导血小板聚集、血小板肿瘤坏死因子-α（TNF-α）受体表达和血清血栓素B-2水平高于20例健康受试者，循环TNF-α水平也高于20例健康受试者。HF患者的血小板与TNF-α受体抑制剂共孵育可显著降低胶原诱导的血小板聚集。体外研究表明，TNF-α放大了血小板对胶原蛋白的反应; TNF-α受体拮抗剂和花生四烯酸代谢抑制剂可抑制这种作用。这项研究表明，TNF-α通过刺激花生四烯酸途径作为血小板活化的触发剂。
The clinical history of patients with heart failure (HF) is complicated by arterial thromboembolism. Platelet activation is reported in this population, but the underlying mechanism has not been clarified. Forty-two patients with HF scored according to New York Heart Association (NYHA) classification had higher levels of collagen-induced platelet aggregation, platelet tumor necrosis factor-alpha (TNF-alpha) receptor expression, and serum thromboxane B-2 and higher circulating levels of TNF-alpha than 20 healthy subjects. Coincubation of platelets from HF patients with an inhibitor of TNF-alpha receptors significantly reduced collagen-induced platelet aggregation. In vitro study demonstrated that TNF-alpha amplified the platelet response to collagen; this effect was inhibited by TNF-alpha receptor antagonist and inhibitors of arachidonic acid metabolism. This study showed that TNF-alpha behaves as a trigger of platelet activation through stimulation of the arachidonic acid pathway.