Juhan-Vague I, Alessi M-C, Mavri A, Morange P E
Laboratory of Hematology, CHU Timone, Inserm Epi 99-36, Marseille, France.
J Thromb Haemost. 2003 Jul;1(7):1575-9. doi: 10.1046/j.1538-7836.2003.00279.x.
Elevated plasma plasminogen activator inhibitor-1 (PAI-1) level is a core feature of insulin-resistance syndrome (IRS). Atherothrombotic complications in IRS are partly attributed to impaired fibrinolysis caused by increased plasma PAI-1 levels. Although the etiology of IRS is far from being explained, the clustering of inflammation, adipose tissue accumulation and insulin resistance suggests an etiopathological link. Proinflammatory cytokines might regulate PAI-1 expression in IRS; however, more studies are needed to confirm this complex mechanism in humans. Furthermore, modifying PAI-1 expression by PAI-1 inhibitors provides a new challenge and may reveal the true role of PAI-1 in atherosclerotic and insulin resistance processes.
血浆纤溶酶原激活物抑制剂-1(PAI-1)水平升高是胰岛素抵抗综合征(IRS)的核心特征。IRS中的动脉粥样血栓形成并发症部分归因于血浆PAI-1水平升高导致的纤维蛋白溶解受损。尽管IRS的病因远未得到解释,但炎症、脂肪组织堆积和胰岛素抵抗的聚集表明存在病因病理联系。促炎细胞因子可能调节IRS中PAI-1的表达;然而,需要更多研究来证实人类中的这一复杂机制。此外,通过PAI-1抑制剂改变PAI-1表达带来了新的挑战,可能揭示PAI-1在动脉粥样硬化和胰岛素抵抗过程中的真正作用。