Inhibition of β-catenin signaling attenuates arteriovenous fistula thickening in mice by suppressing myofibroblasts.

ABSTRACT:

Background

Arteriovenous fistula (AVF) is the most important vascular access for hemodialysis; however, preventive treatment to maintain the patency of AVFs has not been developed. In endothelium, β-catenin functions in both the intercellular adherens complex and signaling pathways that induce the transition of endothelial cells to myofibroblasts in response to mechanical stimuli. We hypothesize that mechanical disturbances in the AVF activate β-catenin signaling leading to the transition of endothelial cells to myofibroblasts, which cause AVF thickening. The present study aimed to test this hypothesis.

Methods

Chronic kidney disease in mice was induced by a 0.2% adenine diet. AVFs were created by aortocaval puncture. Human umbilical vein endothelial cells (HUVECs) were used

SUBMITTER: Liu CT 

PROVIDER: S-EPMC8783463 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature