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The C-terminal domains cause non-L1 GUS enzymes to adopt more open active sites, as opposed to the “C-term-mediated” tetrameric state exhibited by L1 GUS enzymes that create smaller, more intimate active sites (Figs 2b and 3b)

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In this review, we summarize the pathophysiological mechanisms of vascular aging and arterial stiffness, outline the resulting end-organ damage, present different methods for the measurement of arterial stiffness, highlight the potential role of prevention and therapy, and provide future perspectives for arterial stiffness research