Regulation of VWF (Von Willebrand Factor) in Inflammatory Thrombosis.
Xue D ManzHarm Jan BogaardJurjan AmanPublished in: Arteriosclerosis, thrombosis, and vascular biology (2022)
Increasing evidence indicates that inflammation promotes thrombosis via a VWF (von Willebrand factor)-mediated mechanism. VWF plays an essential role in maintaining the balance between blood coagulation and bleeding, and inflammation can lead to aberrant regulation. VWF is regulated on a transcriptional and (post-)translational level, and its secretion into the circulation captures platelets upon endothelial activation. The significant progress that has been made in understanding transcriptional and translational regulation of VWF is described in this review. First, we describe how VWF is regulated at the transcriptional and post-translational level with a specific focus on the influence of inflammatory and immune responses. Next, we describe how changes in regulation are linked with various cardiovascular diseases. Recent insights from clinical diseases provide evidence for direct molecular links between inflammation and thrombosis, including atherosclerosis, chronic thromboembolic pulmonary hypertension, and COVID-19. Finally, we will briefly describe clinical implications for antithrombotic treatment.
Keyphrases
- oxidative stress
- transcription factor
- pulmonary embolism
- cardiovascular disease
- pulmonary hypertension
- immune response
- gene expression
- atrial fibrillation
- coronavirus disease
- sars cov
- metabolic syndrome
- toll like receptor
- cardiovascular risk factors
- pulmonary artery
- cardiovascular events
- red blood cell
- combination therapy
- respiratory syndrome coronavirus