Abstract
Vascular access failure is a major clinical problem for patients on hemodialysis, but therapeutic approaches aimed at improving arteriovenous fistula (AVF) dysfunction remain elusive. Using a murine AVF model, Juncos et al. demonstrate for the first time that the stress protein heme oxygenase-1 (HO-1) is induced in AVFs and that HO-1 is a critical determinant of AVF survival.
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