Despite the formation of a structurally appropriate neoartery the TE50 graft dilation and pulsatility data gathered over 8 months indicated a potential mismatch between the mechanical properties of the native artery and the regenerating graft . Dilation is known to reduce blood flow velocity and generate turbulence , which may limit the durability of the TE50 graft and should be prevented in future studies . This dilation of TE50 could be limited either by chemically modifying PGS [ 7b ] to slow graft degradation or by reinforcing the graft through the addition of an outer sheath layer made from materials previously reported to facilitate collagen production . [ 7c ] The mouse AA and neoarteries regenerated from TE50 grafts comprised similar fractions of elastin and SMCs , as well as a typical endothelium layer , but significantly lower amounts of collagen . It is likely that limited generation of collagen in the graft adventitia was the main contributing factor to graft dilation over time , with the loss of mechanical strength due to the rapid degradation of the original graft not compensated for by adequate collagen deposition . The dilation that the TE50 grafts experienced differs from that seen in aortic aneurysm , which is associated with an increase in collagen content as a response to selective elastin degradation . [ 36 ] Here EL generation occurred at an early stage , but limited collagen regeneration compromised the graft and led to early dilation . This indicates that early and balanced production of both organized elastin and collagen is required for the formation of a mechanically viable neoartery . Various groups have reported the generation of appropriate collagen types and amounts within their vascular graft prototypes and similar strategies could be adopted to improve the TE50 graft . [ 7b , c,22,37 ] The de novo production of organized EL in the intima - media has been identified as the missing element in biodegradable vascular graft regeneration . [ 5,7a ] Most elastogenesis is classically restricted to late fetal and early neonatal periods , [ 38 ] with limited elastin synthesis in adulthood that is in response to the loss of elastin due to injury or disease . [ 39 ] In blood vessels , elastin is an extremely durable insoluble protein and mature elastic fibers generally persist for the lifespan . [ 40 ] Adv . Mater . 2022 , 34 , 2205614 Figure 8 . Proposed remodeling of TE50 . After implantation , the non - porous TE50 vascular graft allows migration of arterial smooth muscle cells ( SMCs ) from adjacent tissue to form intima - media with a circumferential aligned and layered structure . TE is gradually released from the graft . Amorphous elastin and elastin fibers are produced and assembled to form elastic lamellae , possibly with the help of M2 macrophages . The internal elastic lamellae are formed at a later stage through the joined effort of SMCs and endothelial cells . The outer surface encounters both phagocytosis activities from M1 macrophages as well as the deposition and remodeling of collagen fibrils by an interplay of arterial SMCs , fibroblasts , pericytes , and M2 macrophages to form adventitia . Upon complete degradation of TE50 , the adventitia meets intima - media to form the neoartery with spatial and microstructural features that resemble the native artery .