In situ tissue engineering of valves and vessels has emerged as a promising alternative able to overcome the lengthy and costly in vitro procedures of the traditional tissue engineering. The idea of this approach is to fully exploit the body’s regenerative capacity by implanting a cells-free, biodegradable, off-the-shelf available scaffold able to promote the growth and remodelling of new functional tissue.
In particular, tissue-engineered vascular grafts (TEVGs) represent a new paradigm in long-term treatment of end-stage renal-disease patients, since they may have the potential to overcome the major clinical problem related to hemodialysis therapy in both native AVFs (arteriovenous fistula) and synthetic AVGs (arteriovenous graft), that is the vascular access failure due to the formation of neointimal hyperplasia (NIH) at the vein-graft junctions.
NIH is a pathological ongoing remodelling characterized by an excessive proliferation of VSMCs and fibroblast, leading to the intimal thickening of the vein and, later on, to the formation of stenosis.
Nowadays, the pathogenesis of NIH in vascular access grafts is well described, but, although it is strongly believed to be correlated with, among other factors, the fluid wall shear stress (WSS), the exact WSS metric that triggers the onset and development of the disease is not yet known.
In this complex and unknow picture, with this project, we aim in (i) understanding why the NIH is happening in vascular access grafts, in order to (ii) design a novel TE vascular graft that can reduce the occurrence of the pathology, thus reducing vascular access dysfunction in long-term hemodialysis treatment.