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Angiogenesis ; 24(1): 47-55, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-32989644

RESUMO

Peripheral arterial disease occurs more frequently and has a worse prognosis in patients with chronic kidney disease (CKD). The receptor for advanced glycation end products (RAGE) is involved in multiple aspects of uremia-associated vasculopathy. Previous data suggest that the RAGE pathway may promote soluble fms-like tyrosine kinase 1 (sFlt1) production, an anti-angiogenic molecule. Thus, we tested the hypothesis that the deletion of AgeR would decrease sFlt1 production and improve post-ischemic revascularization in uremic condition. We used a well-established CKD model (5/6 nephrectomy) in WT and AgeR-/- C57/Bl6 mice. Hindlimb ischemia was induced by femoral artery ligation. Revascularization was evaluated by complementary approaches: ischemic limb retraction, LASCA imagery, and capillary density. The production of sFlt1 was assessed at both RNA and protein levels. After hindlimb ischemia, uremic mice showed slower functional recovery (p < 0.01), decreased reperfusion (p < 0.01), lower capillary density (p = 0.02), and increased circulating sFlt1 levels (p = 0.03). AgeR deletion restored post-ischemic angiogenesis and was protective from sFlt1 increase in uremic mice. These findings show the main role of RAGE in post-ischemic angiogenesis impairment associated with CKD. RAGE may represent a key target for building new therapeutic approaches to improve the outcome of CKD patients with PAD.


Assuntos
Deleção de Genes , Isquemia/complicações , Neovascularização Fisiológica , Receptor para Produtos Finais de Glicação Avançada/deficiência , Uremia/complicações , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/biossíntese , Animais , Biomarcadores/sangue , Linhagem Celular , Humanos , Ligantes , Masculino , Camundongos Endogâmicos C57BL , RNA/metabolismo , Receptor para Produtos Finais de Glicação Avançada/metabolismo , Solubilidade , Regulação para Cima
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