Abstract
Plaque disruption and subsequent thrombus formation play a critical role in the clinical manifestations of atherothrombosis. Vulnerable lesions are characterized by the existence of core rich in lipid, macrophages and tissue factor (TF). Plaque disruption facilitates the interaction between flowing blood with the inner components (TF) of disrupted atherosclerotic lesions triggering the coagulation cascade. TF, thrombin, platelets, fibrin and inflammatory cells are involved in this process of acute thrombus formation. This pathologic process is significantly accelerated by several "cardiovascular risk factors" such as diabetes, smoking, dyslipemia, etc. We will review on the role of TF, plaque cell apoptosis and blood thrombogenicity acting as a thread of inflammatory and prothrombotic mediators. We will also review the role of activated platelets as source for pro-inflammatory cytokines and enunciation of thrombotic process. Overall, we will try to emphasize the most recent understanding of the concepts involved in the interaction between inflammation and coagulation within the setting of atherothrombotic disease.
Keywords: Atherothrombosis, atherosclerosis, tissue factor, thrombin, platelet, apoptosis, inflammation, thrombosis, plaque, vulnerable plaque
Current Molecular Medicine
Title: Links Between Inflammation and Thrombogenicity in Atherosclerosis
Volume: 6 Issue: 5
Author(s): J. F. Viles-Gonzalez, V. Fuster and J. J. Badimon
Affiliation:
Keywords: Atherothrombosis, atherosclerosis, tissue factor, thrombin, platelet, apoptosis, inflammation, thrombosis, plaque, vulnerable plaque
Abstract: Plaque disruption and subsequent thrombus formation play a critical role in the clinical manifestations of atherothrombosis. Vulnerable lesions are characterized by the existence of core rich in lipid, macrophages and tissue factor (TF). Plaque disruption facilitates the interaction between flowing blood with the inner components (TF) of disrupted atherosclerotic lesions triggering the coagulation cascade. TF, thrombin, platelets, fibrin and inflammatory cells are involved in this process of acute thrombus formation. This pathologic process is significantly accelerated by several "cardiovascular risk factors" such as diabetes, smoking, dyslipemia, etc. We will review on the role of TF, plaque cell apoptosis and blood thrombogenicity acting as a thread of inflammatory and prothrombotic mediators. We will also review the role of activated platelets as source for pro-inflammatory cytokines and enunciation of thrombotic process. Overall, we will try to emphasize the most recent understanding of the concepts involved in the interaction between inflammation and coagulation within the setting of atherothrombotic disease.
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Cite this article as:
Viles-Gonzalez F. J., Fuster V. and Badimon J. J., Links Between Inflammation and Thrombogenicity in Atherosclerosis, Current Molecular Medicine 2006; 6 (5) . https://dx.doi.org/10.2174/156652406778018707
DOI https://dx.doi.org/10.2174/156652406778018707 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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