Investigating mechanisms of chronic kidney disease in mouse models

被引:129
作者
Eddy, Allison A. [1 ,2 ]
Lopez-Guisa, Jesus M. [1 ,2 ]
Okamura, Daryl M. [1 ,2 ]
Yamaguchi, Ikuyo [1 ,2 ]
机构
[1] Seattle Childrens Res Inst, Ctr Tissue & Cell Sci, Seattle, WA 98101 USA
[2] Univ Washington, Dept Pediat, Seattle, WA 98195 USA
基金
美国国家卫生研究院;
关键词
Fibrosis; Collagen; Animal models; Extracellular matrix; Chronic kidney disease; Unilateral ureteral obstruction; UNILATERAL URETERAL OBSTRUCTION; GLOMERULAR-BASEMENT-MEMBRANE; RENAL FIBROSIS; INTERSTITIAL FIBROSIS; MICE LACKING; DIABETIC-NEPHROPATHY; CRESCENTIC GLOMERULONEPHRITIS; MATRIX METALLOPROTEINASES; DEFICIENCY; PROTEIN;
D O I
10.1007/s00467-011-1938-2
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Animal models of chronic kidney disease (CKD) are important experimental tools that are used to investigate novel mechanistic pathways and to validate potential new therapeutic interventions prior to pre-clinical testing in humans. Over the past several years, mouse CKD models have been extensively used for these purposes. Despite significant limitations, the model of unilateral ureteral obstruction (UUO) has essentially become the high-throughput in vivo model, as it recapitulates the fundamental pathogenetic mechanisms that typify all forms of CKD in a relatively short time span. In addition, several alternative mouse models are available that can be used to validate new mechanistic paradigms and/or novel therapies. Here, we review several models-both genetic and experimentally induced-that provide investigators with an opportunity to include renal functional study end-points together with quantitative measures of fibrosis severity, something that is not possible with the UUO model.
引用
收藏
页码:1233 / 1247
页数:15
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