Inhibition of endothelial to mesenchymal transition in a large animal preclinical arterio-venous fistula model leads to improved remodeling and reduced stenosis.
狭窄
医学
间充质干细胞
心脏病学
内科学
病理
作者
Yang Xu,Adam H. Korayem,A.S. Cruz-Solbes,Nirupama Chandel,Tomoki Sakata,Renata Mazurek,Spyros A. Mavropoulos,Taro Kariya,Tadao Aikawa,Kelly P. Yamada,Valentina d’Escamard,Bhargavi V’Gangula,Andrew H. Baker,Lijiang Ma,Johan Björkegren,Valentín Fuster,Manfred Boehm,Kenneth Fish,Rami O. Tadros,Kiyotake Ishikawa,Jason C. Kovacic
Vein grafts are used for many indications, including bypass graft surgery and arterio-venous fistula (AVF) formation. However, patency following vein grafting or AVF formation is suboptimal for various reasons, including thrombosis, neointimal hyperplasia and adverse remodeling. Recently, endothelial to mesenchymal transition (EndMT) was found to contribute to neointimal hyperplasia in mouse vein grafts. We aimed to evaluate the clinical potential of inhibiting EndMT, and developed the first dedicated preclinical model to study the efficacy of local EndMT inhibition immediately prior to AVF creation.