期刊
KIDNEY INTERNATIONAL
卷 74, 期 1, 页码 47-51出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2008.110
关键词
arteriovenous access; arteriovenous fistula; arteriovenous graft; chronic dialysis; heme oxygenase
资金
- NIDDK NIH HHS [DK-70124, R01 DK070124-05, R01 DK070124] Funding Source: Medline
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-beta 1, 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.
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