Von Willebrand factor in inflammation and heart failure: beyond thromboembolic and bleeding risk

Graphical AbstractPotential involvement of von Willebrand factor in the development of heart failure. Von Willebrand factor (vWF) is expressed by endothelial cells and inactivated by the plasma metalloproteinase ADAMTS13 (disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13). The choline transmembrane transporter Slc44A2, expressed on neutrophils' surface recognizes vWF and induces neutrophil extracellular traps extrusion (NETosis). In cardiomyocytes, NETosis induces mitochondrial dysfunction, thus worsening myocardial function. Progression of heart failure is associated with systemic inflammation, and this further induces the endothelial expression of vWF and the inhibition of ADAMTS13. Created with BioRender.com.Open in new tabDownload slide