Thromb Haemost 2008; 99(03): 480-486
DOI: 10.1160/TH07-11-0685
Theme Issue Article
Schattauer GmbH

Platelet-vessel wall interactions in atherosclerotic disease

Harald F. Langer*
1   Medizinische Klinik III, Klinik für Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen, Germany
,
Meinrad Gawaz
1   Medizinische Klinik III, Klinik für Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen, Germany
› Author Affiliations
Financial support: The study was supported by grants of the Deutsche Forschungsgemeinschaft (Graduiertenkolleg GK794, MA121/2–1, Li849/3–1), the Wilhelm Sander-Stiftung (Nr. 2003.0601), the Novartis-Stiftung, the Karl & Lore Klein Stiftung (D.30.08886), the Karl Kuhn Stiftung (AZ III 1.7–0415.221.18–01/AE04/2005), the Bundesministerium fuer Bildung, Wissenschaft, Forschung und Technologie and the fortuene program of the UKT. Dr. Langer received a research grant from the German Cardiac Society (Pfizer Stipendium).
Further Information

Publication History

Received: 16 November 2007

Accepted after major revision: 06 February 2008

Publication Date:
07 December 2017 (online)

Summary

During the prolonged course of atherosclerotic disease,platelets are of central importance as they contribute to the initiation of the disease, to its progression and acute exacerbation but also provide potential regenerative mechanisms. Platelets secrete chemokines and cytokines that mediate vascular inflammation and are in turn activated by substances released from cells of the vascular wall.These interactions represent positive and negative feedback loops, which in case of dysregulation may lead to development and progression of disease. Furthermore, platelet adhesion to the endothelium is critical for the initiation of atherosclerotic lesion formation in vivo. Even prior to endothelial denudation, platelet adhesion governed by disturbed flow at predilection sites for atherosclerosis induces recruitment of proathe- rosclerotic cells and release of proinflammatory mediators from all involved cell types.Finally,the pathogenetic role of platelets for late atheroclerotic events including plaque rupture, microembolism or spasms within the microcirculation is well established. However, increasing evidence indicates that platelets mediate on the other hand potential regenerative mechanisms. Platelets recruit circulating progenitor cells to sites of vascular injury. Furthermore, they influence their biological activity and maturation. Therefore,platelets contribute at all stages of vascular disease by interfering with highly dynamic processes. Understanding interactions of platelets with other circulating cells and the vascular wall is a prerequisite to understand cardiovascular disease and to identify potential therapeutic targets.

Notes

* Currently: Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA


 
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