Abstract
Within many general functions the endothelium is equipped with a number of mechanisms
that prevent thrombus formation in the circulatory system. It harbours factors that
interrupt the coagulation cascade, such as antithrombin III, the protein C receptor
thrombomodulin, and tissue factor pathway inhibitor. It prevents platelet activation
by the production of nitric oxide and prostacyclin, exonucleotidases and surface heparan
sulphates. Furthermore, it can trigger and control fibrinolysis by the synthesis and
release of tissue-type plasminogen activator and its inhibitor PAI-1. The general
properties of the endothelium are subject to adaptation by environmental factors,
such as inflammatory mediators and shear forces. Interleukin-1 and tumour necrosis
factor-α reduce the antithrombotic properties of the endothelium. Furthermore, local
variation exists between different vascular beds and vessel types, such as in the
endometrium. While the endothelium controls blood fluidity on its apical side, adaptation
of the endothelium also prepares its involvement in tissue repair upon inflammation
or damage. The fibrin matrix, which is formed after damage of the vascular system,
not only acts as a sealing of the wound, but also facilitates the repair process by
providing a scaffolding for cell invasion and angiogenesis.
Keywords
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© 2001 Elsevier Science Ireland Ltd. Published by Elsevier Inc. All rights reserved.
