Could Notch signaling pathway be a potential therapeutic option in renal diseases?

被引:11
|
作者
Marquez-Exposito, Laura [1 ]
Cantero-Navarro, Elena [1 ]
Lavoz, Carolina [2 ]
Fierro-Fernandez, Marta [3 ]
Poveda, Jonay [1 ]
Rayego-Mateos, Sandra [1 ]
Rodrigues-Diez, Raul R. [4 ]
Luis Morgado-Pascual, Jose [1 ]
Orejudo, Macarena [1 ]
Mezzano, Sergio [2 ]
Ruiz-Ortega, Marta [1 ]
机构
[1] Univ Autonoma Madrid, Fdn Jimenez Diaz, Lab Biol Celular Enfermedades Renales, IIS, Madrid, Spain
[2] Univ Austral Chile, Fac Med, Div Nefrol, Valdivia, Chile
[3] Ctr Biol Mol Severo Ochoa, Madrid, Spain
[4] Idipaz, Madrid, Spain
来源
NEFROLOGIA | 2018年 / 38卷 / 05期
关键词
Notch; Renal damage; Mechanisms; Fibrosis; Inflammation; NF-KAPPA-B; ACUTE KIDNEY INJURY; DIABETIC-NEPHROPATHY; FIBROSIS DEVELOPMENT; ACTIVATION; GREMLIN; INFLAMMATION; GLOMERULOSCLEROSIS; ATHEROSCLEROSIS; DIFFERENTIATION;
D O I
10.1016/j.nefro.2017.11.027
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Notch pathway regulates key processes in the kidney, involved in embryonic development and tissue damage. In many human chronic renal diseases a local activation of Notch pathway has been described, suggesting that several components of Notch pathway could be considered as biomarkers of renal damage. Experimental studies by genetic modulation of Notch components or pharmacological approaches by gamma-secretase inhibitors have demonstrated the role of this pathway in renal regeneration renal, podocyte apoptosis, proliferation and fibroblasts activation, and induction of epithelial to mesenchymal transition of tubular epithelial cells. Recent studies suggest an interaction between Notch and NF-kappa B pathway involved in the regulation of renal inflammatory process. On the other hand, there are some miRNAs that could regulate Notch components and down-stream responses. All these data suggest that Notch blockade could be a novel therapeutic option for renal diseases. (c) 2018 Sociedad Espanola de Nefrologia. Published by Elsevier Espana, S.L.U. This is an open access article under the CC BY-NC-ND license.
引用
收藏
页码:466 / 475
页数:10
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