TY - JOUR
T1 - Regulation of VWF (Von Willebrand Factor) in Inflammatory Thrombosis
AU - Manz, Xue D.
AU - Bogaard, Harm Jan
AU - Aman, Jurjan
N1 - Funding Information: X.D. Manz is funded by a research grant from the Institute for CardioVascular Research (ICaR-VU) at the VU University Medical Center, Amsterdam, the Netherlands. Publisher Copyright: © 2022 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2022/11/1
Y1 - 2022/11/1
N2 - 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.
AB - 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.
KW - COVID-19
KW - cardiovascular diseases
KW - chronic thromboembolic pulmonary hypertension
KW - inflammation
KW - thrombosis
KW - von Willebrand factor
UR - http://www.scopus.com/inward/record.url?scp=85140857033&partnerID=8YFLogxK
U2 - https://doi.org/10.1161/ATVBAHA.122.318179
DO - https://doi.org/10.1161/ATVBAHA.122.318179
M3 - Review article
C2 - 36172866
SN - 1079-5642
VL - 42
SP - 1307
EP - 1320
JO - Arteriosclerosis, Thrombosis, and Vascular Biology
JF - Arteriosclerosis, Thrombosis, and Vascular Biology
IS - 11
ER -