Research Paper Volume 16, Issue 11 pp 9876—9898
High estrogen induces trans-differentiation of vascular smooth muscle cells to a macrophage-like phenotype resulting in aortic inflammation via inhibiting VHL/HIF1a/KLF4 axis
Figure 7. Mechanism of estrogen-induced conversion of VSMCs to a macrophage-like phenotype leading to inflammation in mouse aorta. Upon binding to its receptor, estrogen inhibits the binding of VHL/VBC. VHL induces both ubiquitination degradation of KLF4 and acts to hydrolyze HIF-1α. When VHL expression is reduced, KLF4 expression rises, which in turn enters the nucleus and participates in the phenotype of vascular smooth muscle cells. Created with BioRender.