Thrombosis is a deadly medical complication, yet the management of thrombosis is still not satisfactory. Traditionally, platelet activation on the injured blood vessel wall is considered to be the pathogenesis for arterial thrombosis, while the increased coagulation and vascular inflammation contribute to the initiation of venous thrombosis. Thus, antiplatelet and anticoagulant therapeutics are the main treatment for arterial and venous thrombosis.
Increasing numbers of studies indicate that immune responses and coagulation could be a causal factor in arterial thrombosis. For example, increased myocardial infarction during infection of respiratory viruses may be due to host elevation of coagulation and inflammation factors. Alternatively, inflamed leukocytes may facilitate venous thrombosis through activating platelets which enhances coagulation. For these reasons, arterial and venous thrombosis should not be viewed as two different entities. Further understanding of the crosstalk between inflammation and and thrombosis within two types of blood vessels will benefit the development of more effective and safer anti-thrombosis treatments.
Led by a team of subject experts, this Research Topic will explore the role of inflammation in venous and arterial thrombosis. Sub-topics include, but are not limited to:
- Pro-coagulation functions of platelets in arterial thrombosis
- Platelets in the initiation of venous thrombo-embolism during viral infection
- Immune responses of leukocytes in arterial thrombosis during viral infection
Thrombosis is a deadly medical complication, yet the management of thrombosis is still not satisfactory. Traditionally, platelet activation on the injured blood vessel wall is considered to be the pathogenesis for arterial thrombosis, while the increased coagulation and vascular inflammation contribute to the initiation of venous thrombosis. Thus, antiplatelet and anticoagulant therapeutics are the main treatment for arterial and venous thrombosis.
Increasing numbers of studies indicate that immune responses and coagulation could be a causal factor in arterial thrombosis. For example, increased myocardial infarction during infection of respiratory viruses may be due to host elevation of coagulation and inflammation factors. Alternatively, inflamed leukocytes may facilitate venous thrombosis through activating platelets which enhances coagulation. For these reasons, arterial and venous thrombosis should not be viewed as two different entities. Further understanding of the crosstalk between inflammation and and thrombosis within two types of blood vessels will benefit the development of more effective and safer anti-thrombosis treatments.
Led by a team of subject experts, this Research Topic will explore the role of inflammation in venous and arterial thrombosis. Sub-topics include, but are not limited to:
- Pro-coagulation functions of platelets in arterial thrombosis
- Platelets in the initiation of venous thrombo-embolism during viral infection
- Immune responses of leukocytes in arterial thrombosis during viral infection
