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ABSTRACT: Background
Arteriovenous fistulae (AVF) are the gold standard for vascular access for hemodialysis. Although the vein must thicken and dilate for successful hemodialysis, excessive wall thickness leads to stenosis causing AVF failure. Since TGF-β (transforming growth factor-beta) regulates ECM (extracellular matrix) deposition and smooth muscle cell (SMC) proliferation-critical components of wall thickness-we hypothesized that disruption of TGF-β signaling prevents excessive wall thickening during venous remodeling.Methods
A mouse aortocaval fistula model was used. SB431542-an inhibitor of TGF-β receptor I-was encapsulated in nanoparticles and applied to the AVF adventitia in C57BL/6J mice. Alternatively, AVFs were created in mice with conditional disruption of TGF-β recept
SUBMITTER: Taniguchi R
PROVIDER: S-EPMC9233042 | biostudies-literature | 2022 Jul
REPOSITORIES: biostudies-literature