| First Author | Juncos JP | Year | 2008 |
| Journal | Kidney Int | Volume | 74 |
| Issue | 1 | Pages | 47-51 |
| PubMed ID | 18368029 | Mgi Jnum | J:152953 |
| Mgi Id | MGI:4360458 | Doi | 10.1038/ki.2008.110 |
| Citation | Juncos JP, et al. (2008) Genetic deficiency of heme oxygenase-1 impairs functionality and form of an arteriovenous fistula in the mouse. Kidney Int 74(1):47-51 |
| abstractText | 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 PDGF alpha, IGF-1, TGF-beta1, 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. |
