Figure 1.
Pathophysiology underlying low VWF levels. Hepatic macrophages, liver sinusoidal ECs (LSECs), and hepatocytes contribute to regulating VWF clearance. A number of cell surface receptors have also been described. On LSECs these include stabilin-2 (STAB2) and C-type lectin domain family 4 member M (CLEC4M). Macrophage receptors include Siglec-5, the low-density lipoprotein receptor-related protein-1 (LRP1), the scavenger receptor class A member I (SR-A1), and macrophage galactose-type lectin (MGL). Finally, the asialoglycoprotein receptor (ASGPR) on hepatocytes has also been implicated. PTM, posttranslational modification.

Pathophysiology underlying low VWF levels. Hepatic macrophages, liver sinusoidal ECs (LSECs), and hepatocytes contribute to regulating VWF clearance. A number of cell surface receptors have also been described. On LSECs these include stabilin-2 (STAB2) and C-type lectin domain family 4 member M (CLEC4M). Macrophage receptors include Siglec-5, the low-density lipoprotein receptor-related protein-1 (LRP1), the scavenger receptor class A member I (SR-A1), and macrophage galactose-type lectin (MGL). Finally, the asialoglycoprotein receptor (ASGPR) on hepatocytes has also been implicated. PTM, posttranslational modification.

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