作者: Anak Agung , Gde Budhiarta
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摘要: Plasminogen can be converted to plasmin either by t-PA or u-PA. A dual role for these pathways is now well established where involved in fibrin homeostasis and u-PA primarily cell migration tissue remodelling. Using this mechanism thrombolytic terapy of myocardial infarction some other thromboembolic diseases have been introduced. Thrombolytic therapy could improved earlier accelerated treatment, the used plasminogen activator with increased potency such as reteplase, tenetecplase staphylokinase use more specific potent anticoagulant antiplatelet agents. Increased activity matrix metalloproteinases (MMPs) has implicated numerous disease processes, including tumor growth metastases, arthritis, periodontal disease. It becoming increasingly clear that extracelluler degradation M Ps also pathogenesis cardiovascular disease, atherosclerosis, restenosis, dilated cardiomyapathi,and infarction. Administration synthetic MMP inhibitor experimental animal models of; significantly inhibits progression respectivelyatherosclerotic lesion formation, neointima left ventricular remodeling, pump dysfunction, infarc healing.