A similar increase in ADAMTS-1 was observed in aortas of AngII-treated Adamts5<sup>Δcat</sup> mice but was not sufficient to maintain versican processing and prevent aortic dilatation.
It is proposed that the decreased synthesis and increased degradation of versican, particularly of isoform V(0), and the resulting low concentration in the intima are crucial factors contributing to the altered viscoelastic and compressive properties and thereby to the deformity and dilatation of aorta.