The role of inflammatory cytokines in endothelial dysfunction.

The role of inflammatory cytokines in endothelial dysfunction.
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DOI:
10.1007/s00395-008-0733-0
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发表时间:
2008-09
影响因子:
9.5
通讯作者:
Zhang C
Zhang C
中科院分区:
医学1区
文献类型:
--
作者:
Zhang C

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临床和实验数据支持内皮功能障碍和炎症之间的联系。炎症细胞因子是动脉粥样硬化斑块形成的重要主角,对整个动脉粥样硬化血管产生影响。重要的是,无论危险因素如何,例如糖尿病、高血压、肥胖,动脉粥样硬化病变的发展的特征都是内皮细胞正常功能的破坏。内皮细胞排列在脉管系统的内腔中,是调节血管舒张和血管收缩、血管平滑肌细胞生长、炎症和止血、维持组织适当的血液供应并调节炎症和凝血的复杂系统的一部分。目前的概念表明,动脉粥样硬化形成的最早事件是内皮功能障碍,表现为一氧化氮(NO)和前列环素的产生不足。本综述的重点是总结最近的证据,显示炎症对缺血性心脏病血管功能障碍的影响,这可能会为未来治疗中针对炎症的新方向提供新的方向。
Clinical and experimental data support a link between endothelial dysfunction and inflammation. Inflammatory cytokines are important protagonists in formation of atherosclerotic plaque, eliciting effects throughout the atherosclerotic vessel. Importantly, the development of atherosclerotic lesions, regardless of the risk factor, e.g., diabetes, hypertension, obesity, is characterized by disruption in normal function of the endothelial cells. Endothelial cells, which line the internal lumen of the vasculature, are part of a complex system that regulates vasodilation and vasoconstriction, growth of vascular smooth muscle cells, inflammation, and hemostasis, maintaining a proper blood supply to tissues and regulating inflammation and coagulation. Current concepts suggest that the earliest event in atherogenesis is endothelial dysfunction, manifested by deficiencies in the production of nitric oxide (NO) and prostacyclin. The focus of this review is to summarize recent evidence showing the effects of inflammation on vascular dysfunction in ischemic-heart disease, which may prompt new directions for targeting inflammation in future therapies.
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