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Review
. 2008 Jul;74(1):9-11.
doi: 10.1038/ki.2008.127.

HOming in on arteriovenous fistula survival

W Durante  1 , C-C Lin
Affiliations
Review

HOming in on arteriovenous fistula survival

W Durante et al. Kidney Int. 2008 Jul.

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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Figures

Figure 1
Figure 1
Model for the protective role of heme oxygenase-1 (HO-1) in arteriovenous fistula (AVF) failure. Several factors (surgical injury, oxidative stress, inflammatory stress, and hemodynamic stress) associated with the creation of an AVF leads to the induction of HO-1 in the fistula. HO-1 mediates the oxidative metabolism of heme to carbon monoxide (CO), iron (Fe), and biliverdin. Subsequently, biliverdin is converted to bilirubin, while iron stimulates ferritin expression. These HO-1 products possess potent antiproliferative, antithrombotic, anti-inflammatory, antifibrotic, antioxidant, and vasodilatory effects that limit AVF stenosis.
See this image and copyright information in PMC

Comment on

References

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    1. Juncos JP, Tracz MJ, Croatt AJ, et al. Genetic deficiency of HO-1 markedly impairs the functionality and form of an arteriovenous fistula in the mouse. Kidney Int. 2007 In press. - PMC - PubMed

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