Prof. Lina Badimon, Cardiovascular Research Center, C/ Sant Antoni Mª Claret 167, 08025 Barcelona, Spain, Tel. +34/93/556 58 80; Fax +34/93/556 55 59, E-mail:
Hamostaseologie. 2013;33(4):259-68. doi: 10.5482/HAMO-13-07-0034.
A link between obesity and coronary artery disease development has been repeatedly proposed, possibly in part due to the development of a proinflammatory and prothrombotic state in obese subjects. Adipocytes secrete numerous hormones and cytokines (adipokines) which influence gene expression and cell functions in endothelial cells, arterial smooth muscle cells, and monocytes/macrophages favouring the development of an atherosclerotic vulnerable plaque. Moreover, the release of such biologically active molecules also promotes endothelial function impairment, disturbs the haemostatic and fibrinolytic systems, and produces alterations in platelet function affecting the initiation, progression, and stabilization of thrombus formation upon atherosclerotic plaque rupture. In this review we will discuss the pathophysiological mechanisms by which obesity contributes to increase atherothrombosis paying special attention to its effects over thrombosis.
肥胖与冠状动脉疾病发展之间存在关联，这一观点已被反复提出，其部分原因可能是肥胖人群体内会产生促炎和促血栓形成状态。脂肪细胞会分泌多种激素和细胞因子（脂肪因子），这些物质会影响内皮细胞、动脉平滑肌细胞和单核细胞/巨噬细胞中的基因表达和细胞功能，从而促进动脉粥样硬化易损斑块的形成。此外，这些具有生物活性的分子的释放还会促进内皮功能障碍，扰乱止血和纤维蛋白溶解系统，并改变血小板功能，影响在动脉粥样硬化斑块破裂时血栓形成的启动、进展和稳定。在本篇综述中，我们将讨论肥胖导致动脉血栓形成风险增加的病理生理机制，特别关注其对血栓形成的影响。
