Pathophysiology of atherothrombosis: Mechanisms of thrombus formation on disrupted atherosclerotic plaques
-
- Yujiro Asada
- Pathophysiology Section, Department of Pathology, Faculty of Medicine University of Miyazaki Miyazaki Japan
-
- Atsushi Yamashita
- Pathophysiology Section, Department of Pathology, Faculty of Medicine University of Miyazaki Miyazaki Japan
-
- Yuichiro Sato
- Department of Diagnostic Pathology, University of Miyazaki Hospital University of Miyazaki Miyazaki Japan
-
- Kinta Hatakeyama
- Department of Diagnostic Pathology Nara Medical University Nara Japan
書誌事項
- 公開日
- 2020-03-13
- 資源種別
- journal article
- 権利情報
-
- http://creativecommons.org/licenses/by-nc/4.0/
- DOI
-
- 10.1111/pin.12921
- 公開者
- Wiley
この論文をさがす
説明
<jats:p>Atherothrombosis is a leading cause of cardiovascular mortality and morbidity worldwide. The underlying mechanisms of atherothrombosis comprise plaque disruption and subsequent thrombus formation. Arterial thrombi are thought to mainly comprise aggregated platelets as a result of high blood velocity. However, thrombi that develop on disrupted plaques comprise not only aggregated platelets, but also large amounts of fibrin, because plaques contain large amount of tissue factor that activate the coagulation cascade. Since not all thrombi grow large enough to occlude the vascular lumen, the propagation of thrombi is also critical in the onset of adverse vascular events. Various factors such as vascular wall thrombogenicity, local hemorheology, systemic thrombogenicity and fibrinolytic activity modulate thrombus formation and propagation. Although the activation mechanisms of platelets and the coagulation cascade have been intensively investigated, the underlying mechanisms of occlusive thrombus formation on disrupted plaques remain obscure. Pathological findings derived from humans and animal models of human atherothrombosis have uncovered pathophysiological processes during thrombus formation and propagation after plaque disruption, and novel factors have been identified that modulate the activation of platelets and the coagulation cascade. These findings have also provided insights into the development of novel drugs for atherothrombosis.</jats:p>
収録刊行物
-
- Pathology International
-
Pathology International 70 (6), 309-322, 2020-03-13
Wiley
