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Atherosclerosis: coagulation and fibrinolysis
K Sueishi1, K Ichikawa, K Kato
1Department of Pathology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Seminars in Thrombosis and Hemostasis
|August 13, 1998
Summary
Tissue factor (TF) and APO(a) contribute to atherosclerosis by promoting fibrin deposition in arterial lesions. This process involves hypercoagulability and hypofibrinolysis, potentially impacting smooth muscle cell proliferation and disease progression.
Area of Science:
- Cardiovascular Biology
- Thrombosis and Hemostasis
- Atherosclerosis Research
Background:
- Tissue factor (TF) is overexpressed in atherosclerotic lesions by macrophages and smooth muscle cells (SMCs).
- APO(a) is found in the stroma and macrophages within atherosclerotic plaques.
- Fibrin deposition increases with lesion severity and co-localizes with TF and APO(a).
Purpose of the Study:
- To investigate the role of TF and APO(a) in fibrin deposition within atherosclerotic lesions.
- To explore the contribution of coagulation and fibrinolysis systems to atherosclerosis initiation and progression.
- To examine the potential impact on smooth muscle cell proliferation and TGF-beta activation.
Main Methods:
- Immunohistochemical localization of TF and APO(a) in atherosclerotic intimas.
- Assessment of fibrin deposition in early versus advanced atherosclerotic lesions.
- Correlation analysis of TF, APO(a), and fibrin deposition with lesion characteristics.
Main Results:
- TF and APO(a) are deposited in the extracellular matrix of atherosclerotic lesions.
- Fibrin deposition is more prevalent in advanced lesions and co-localizes with TF and APO(a).
- These findings suggest a role for coagulation and fibrinolysis in atherosclerosis progression and SMC proliferation.
Conclusions:
- Coagulation and fibrinolysis systems, through fibrin deposition, are crucial in atherosclerosis initiation and progression.
- Neointimal hypercoagulability and hypofibrinolysis contribute to fibrin deposition in plaques and on the arterial surface.
- TF and APO(a) may influence SMC proliferation via altered TGF-beta activation, offering potential therapeutic targets.