Mechanisms of thrombosis in obesity.
Mechanisms of thrombosis in obesity.
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DOI：
10.1097/moh.0b013e3283634443
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发表时间：
2013-09
影响因子：
3.2
通讯作者：
Lentz SR
中科院分区：
文献类型：
--
作者：
Blokhin IO;Lentz SR
肥胖已成为一种世界性流行病，其导致血栓性疾病如心肌梗死、中风和静脉血栓栓塞的发病率和死亡率增加。对肥胖患者血栓形成的有效预防和治疗受限于对潜在血栓形成机制的不完全理解以及对该患者人群中抗凝药物的风险、获益和剂量的不确定性。这篇综述总结了我们目前对肥胖诱导的血栓前状态的既定和新出现的机制的理解。慢性炎症和纤维蛋白溶解受损介导肥胖相关血栓形成的机制影响突出。最近的数据表明脂肪因子和microRNA的异常表达，这似乎是在肥胖症的促炎症和促血栓通路的关键调制器的功能，也进行了审查。最后，一些挑战和新的方法来预防和管理血栓性疾病的肥胖和超重患者进行了讨论。肥胖驱动的慢性炎症和受损的纤维蛋白溶解似乎是肥胖患者血栓形成的主要效应机制。脂肪因子和microRNA的表达和分泌失调可能会加剧肥胖的促炎和纤溶功能减退作用，这进一步增加了血栓形成的风险，并提出了新的潜在治疗靶点。
Obesity has become a worldwide epidemic that is driving increased morbidity and mortality from thrombotic disorders such as myocardial infarction, stroke, and venous thromboembolism. Effective prevention and treatment of thrombosis in obese patients is limited by an incomplete understanding of the underlying prothrombotic mechanisms and by uncertainties about risks, benefits, and dosing of anticoagulant drugs in this patient population. This review summarizes our current understanding of established and emerging mechanisms contributing to the obesity-induced prothrombotic state. The mechanistic impact of chronic inflammation and impaired fibrinolysis in mediating obesity-associated thrombosis is highlighted. Recent data demonstrating the aberrant expression of adipokines and microRNAs, which appear to function as key modulators of proinflammatory and prothrombotic pathways in obesity, are also reviewed. Finally, some challenges and new approaches to the prevention and management of thrombotic disorders in obese and overweight patients are discussed. Obesity-driven chronic inflammation and impaired fibrinolysis appear to be major effector mechanisms of thrombosis in obesity. The proinflammatory and hypofibrinolytic effects of obesity may be exacerbated by dysregulated expression and secretion of adipokines and microRNAs, which further increase the risk of thrombosis and suggest new potential targets for therapy.