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- W972912605 abstract "Fibrinolysis plays critical roles in the clearance of fibrin clots in vasculature, tissue modeling, embryo development and wound healing. Reduced fibrinolytic activity has been frequently found in patients with ischemic heart disease (IHD) and diabetes mellitus. Dys-lipoproteinemia, characterized by increased low density lipoprotein (LDL), very low density lipoprotein (VLDL), lipoprotein (a) [Lp(a)] and decreased high density lipoprotein (HDL), is a common biochemical finding in IHD and diabetes. Previous studies by other groups and ours demonstrated that LDL, VLDL, Lp(a) and their oxidatively modified forms increased the generation of plasminogen activator inhibitor-1 (PAI-1), the major physiological inhibitor for fibrinolysis, from vascular endothelial cells (EC). LDL and Lp(a) reduced the release of tissue plasminogen activator (tPA) from EC. Our group recently demonstrated that glycation enhanced the effects of LDL and Lp(a) on the generation of fibrinolytic regulators from EC. Co-treatment with antixidants or HDL may normalize glycated LDL-induced changes in the fibrinolytic regulators from EC. LDL and VLDL isolated from diabetic patients induced greater increases in PAI-1 generation and further decreased tPA release from EC compared corresponding lipoproteins from healthy subjects. VLDL-responsive element was found in —672/—657 bp region of the PAI-1 promoter. The activation of PKC-s isoform is required for LDL, Lp(a) and their oxidized forms induced PAI-1 production in EC. This review sum-maries the recent findings on the impact and regulatory mechanism for lipoproteins-induced production of fibrinolytic regulators in vascular cells." @default.
- W972912605 created "2016-06-24" @default.
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- W972912605 date "2003-01-01" @default.
- W972912605 modified "2023-09-26" @default.
- W972912605 title "Dyslipoproteinemia and Fibrinolysis" @default.
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- W972912605 doi "https://doi.org/10.1007/978-1-4419-9232-1_23" @default.
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