Abstract
Vascular access dysfunction contributes to patient morbidity during maintenance hemodialysis. In this study we determined if knockout of heme oxygenase-1 predisposed to malfunction of arteriovenous fistulas. After three weeks, all fistulas in wild type mice were patent whereas a third of the fistulas in knockout mice were occluded and these exhibited increased neointimal hyperplasia and venous wall thickening. Heme oxygenase-1 mRNA and protein were robustly induced in the fistulas of the wild type mice. In the knockout mice there was increased PAI-1 and MCP-1 expression, marked induction of MMP-2 and MMP-9, but similar expression of PDGFα, IGF-1, TGF-β1, VEGF, and osteopontin compared to wild type mice. We conclude that heme oxygenase-1 deficiency promotes vasculopathic gene expression, accelerates neointimal hyperplasia and impairs the function of arteriovenous fistulas.
Original language | English (US) |
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Pages (from-to) | 47-51 |
Number of pages | 5 |
Journal | Kidney international |
Volume | 74 |
Issue number | 1 |
DOIs | |
State | Published - Jul 2008 |
Keywords
- Arteriovenous access
- Arteriovenous fistula
- Arteriovenous graft
- Chronic dialysis
- Heme oxygenase
ASJC Scopus subject areas
- Nephrology