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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
The hemostatic system as a regulator of inflammation in atherosclerosis
1Institute of Clinical Biochemistry and Pathobiochemistry, University Hospital Würzburg, Würzburg, Germany.
Insights
The coagulation system significantly impacts atherosclerosis development. Key coagulation factors, like FX, thrombin, and FXIII, regulate inflammation and immunity, offering potential new treatments for cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Inflammation and Immunology
- Hemostasis and Thrombosis
Background:
- Atherosclerosis is a chronic inflammatory arterial disease.
- The coagulation system intricately interacts with inflammation in atherosclerosis.
- Evidence suggests coagulation factors play a crucial role in atherosclerotic lesion development and progression.
Purpose of the Study:
- To review the presence and impact of coagulation factors in atherosclerotic lesions.
- To explore the roles of hypercoagulability and hypocoagulability in lesion formation.
- To discuss the non-hemostatic and immune-modulatory functions of FX, thrombin, and FXIII in atherosclerosis.
Main Methods:
- Literature review of coagulation factors in atherosclerotic lesions.
- Analysis of the unifying common pathway of coagulation.
- Examination of the functions of FX, thrombin, and FXIII in cellular and immune regulation within atherosclerosis.
Main Results:
- Coagulation factors are present in atherosclerotic lesions.
- Both hypercoagulability and hypocoagulability influence atherosclerotic lesion formation.
- FX, thrombin, and FXIII exhibit significant non-hemostatic roles in regulating inflammation and immunity in various cell types.
Conclusions:
- The coagulation system is a critical regulator of inflammation in atherosclerosis.
- Non-hemostatic functions of coagulation factors present therapeutic targets for cardiovascular disease.
- Understanding these roles may lead to novel treatment strategies for atherosclerosis.
Abstract:
Atherosclerosis is a chronic inflammatory disease of the arterial vessel wall. As part of a tightly connected cross-talk between inflammation and coagulation, there is growing evidence that the coagulation system plays a pivotal role in the development and progression of atherosclerosis. We here discuss the presence of coagulation factors in atherosclerotic lesions and the overall effects of hypercoagulability and hypocoagulability on atherosclerotic lesion formation. Moreover, we focus on the unifying common pathway of coagulation, which can be initiated by the intrinsic and extrinsic pathway of coagulation, and discuss the functions of the coagulation factors FX, thrombin, and FXIII as regulators of inflammation in atherosclerosis. In particular, we review the non-hemostatic and immune-modulatory functions of these factors in endothelial and smooth muscle cells, as well as monocytes/macrophages, but also other cells, such as dendritic cells and T cells, that may control the inflammatory process of atherosclerosis. Their multiple roles in coagulation, but also their non-hemostatic functions in different cell types in inflammation and immunity, may harbor great potential for the development of novel therapeutic approaches for treating cardiovascular disease.
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