Figure 1.
Figure 1. Schematic representation of the plasminogen (fibrinolytic) system. / The proenzyme, plasminogen, is converted to the active enzyme plasmin by tissue-type plasminogen activator (t-PA) or by urokinase-type plasminogen activator (u-PA), which binds to a cellular u-PA receptor (u-PAR). Plasmin degrades fibrin and can convert latent matrix metalloproteinases (pro-MMPs) into active MMPs, which in turn degrade extracellular matrix (ECM). Pro-MMPs may also be activated directly by u-PA, or by other MMP. t-PA mediated plasminogen activation is primarily involved in fibrin homeostasis, while plasmin generation via u-PA, complexed with u-PAR plays a role in tissue remodeling. Inhibition may occur at the level of the plasminogen activators by plasminogen activator inhibitors (mainly PAI-1 and possibly PAI-2), at the level of plasmin by α2-antiplasmin and at the level of the MMPs by tissue inhibitors of MMP's (TIMPs).

Schematic representation of the plasminogen (fibrinolytic) system.

The proenzyme, plasminogen, is converted to the active enzyme plasmin by tissue-type plasminogen activator (t-PA) or by urokinase-type plasminogen activator (u-PA), which binds to a cellular u-PA receptor (u-PAR). Plasmin degrades fibrin and can convert latent matrix metalloproteinases (pro-MMPs) into active MMPs, which in turn degrade extracellular matrix (ECM). Pro-MMPs may also be activated directly by u-PA, or by other MMP. t-PA mediated plasminogen activation is primarily involved in fibrin homeostasis, while plasmin generation via u-PA, complexed with u-PAR plays a role in tissue remodeling. Inhibition may occur at the level of the plasminogen activators by plasminogen activator inhibitors (mainly PAI-1 and possibly PAI-2), at the level of plasmin by α2-antiplasmin and at the level of the MMPs by tissue inhibitors of MMP's (TIMPs).

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