Hamostaseologie 2004; 24(01): 1-11
DOI: 10.1055/s-0037-1619601
Grußwort
Schattauer GmbH

Platelet and von Willebrand factor interactions at the vessel wall

Wechselwirkungen an der Zellwand zwischen Thrombozyten und von-Willebrand-Faktor
Z. M. Ruggeri
1   Roon Center for Arteriosclerosis and Thrombosis, Division of Experimental Hemostasis and Thrombosis, Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California, USA
› Author Affiliations
Further Information

Publication History

Publication Date:
22 December 2017 (online)

Summary

The process of platelet thrombus formation contributes to the haemostatic response that prevents excessive blood loss after tissue injury, but may become a life-threatening disease mechanism by causing the acute thrombotic occlusion of atherosclerotic arteries. The participation of platelets in the formation of thrombi is centered on their adhesive properties and the ability to respond to stimuli with rapid activation. Platelet adhesion and activation are multifaceted and modulated by different environmental conditions, suggesting that it should be possible to obtain a selective pharmacological inhibition of the pathways more relevant to atherothrombosis than to haemostasis. In particular, progress in understanding the structure and function of von Willebrand factor and the mechanisms that underlie its interactions with vascular surfaces and platelets can elucidate important differentiating aspects of normal haemostasis and pathological arterial thrombosis.

Zusammenfassung

Die Ausbildung eines Plättchenthrombus dient einerseits der Blutstillung und verhindert bedrohliche Blutverluste nach Verletzung, kann jedoch andererseits durch akute Verschlüsse arteriosklerotischer Arterien zu lebensbedrohlichen Komplikationen führen. Die wichtigsten Eigenschaften der Thrombozyten bei der Thrombusbildung sind ihre Fähigkeit zu adhärieren und ihre Möglichkeit, durch adäquate Stimuli sehr rasch aktiviert zu werden. Adhäsion und Aktivierung werden durch mehrere unabhängige Mechanismen hervorgerufen und unterliegen der Modulation durch unterschiedliche exogene Faktoren. Daher ist es theroretisch möglich, Aktivierungswege pharmakologisch zu beeinflussen, die zu thromboembolischen Komplikationen führen, ohne ihre hämostatische Eigenschaften zu sehr zu kompromittieren. Hierbei sind Fortschritte, die zum besseren Verständnis von Struktur/Wirkungsbeziehungen des von-Willebrand-Faktors und von Mechanismen seiner Interaktion mit Gefäßwänden und Thrombozyten führen, wichtige Meilensteine auf dem Weg, sowohl die normale Hämostase zu erhalten als auch lebensgefährliche Gefäßverschlüsse möglichst zu verhindern.

 
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