期刊
METABOLIC BRAIN DISEASE
卷 32, 期 3, 页码 667-673出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11011-017-0007-3
关键词
Plasminogen activator inhibitor; Obesity; Stroke
资金
- National Natural Science Foundation of China [81670405, 81370409, 81400208, 81400269]
- Natural Science Foundation of Jiangsu Province [BK20161355]
- Social Development Foundation of Zhenjiang [SH2014025]
- Key Laboratory of Cardiovascular Disease of Zhenjiang [SS2012002]
One of the global socioeconomic phenomena occurred during the last decades is the increased prevalence of obesity, with direct consequence on the risk of developing thrombotic disorders. As the physiological inhibitor of tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA), plasminogen activator inhibitor-1 (PAI-1) is well known for its role in fibrinolysis. More and more evidences have shown that PAI-1 involves in physiopathologic mechanisms of many diseases and metabolic disorder. Increased serum level of PAI-1 has been observed in obesity and it also contributes to the development of adipose tissue and then has effects on obesity. Meantime, obesity affects also the PAI-1 levels. These evidences indicate the complicated interaction between PAI-1 and obesity. Many clinic studies have confirmed that obesity relates to the stroke outcome although there are many contradictory results. Simultaneously, correlation is found between plasma PAI-1 and thrombotic cerebrovascular diseases. This article reviews contemporary knowledge regarding the complex interplay of obesity, PAI-1 and stroke.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据