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本文引用的文献

1
Vascular endothelial cadherin modulates renal interstitial fibrosis.血管内皮钙黏蛋白调节肾间质纤维化。
Nephron Exp Nephrol. 2012;120(1):e20-31. doi: 10.1159/000332026. Epub 2011 Nov 25.
2
Vitronectin accumulates in the interstitium but minimally impacts fibrogenesis in experimental chronic kidney disease.纤连蛋白在间质中积累,但对实验性慢性肾脏病的纤维化影响极小。
Am J Physiol Renal Physiol. 2011 May;300(5):F1244-54. doi: 10.1152/ajprenal.00701.2010. Epub 2011 Jan 26.
3
Control of mammalian kidney development by the Hedgehog signaling pathway.Hedgehog 信号通路对哺乳动物肾脏发育的调控。
Pediatr Nephrol. 2011 Sep;26(9):1365-71. doi: 10.1007/s00467-010-1704-x. Epub 2010 Dec 15.
4
The development of atypical hemolytic uremic syndrome depends on complement C5.非典型溶血性尿毒症综合征的发展依赖于补体 C5。
J Am Soc Nephrol. 2011 Jan;22(1):137-45. doi: 10.1681/ASN.2010050451. Epub 2010 Dec 9.
5
Navigating the challenges of fibrosis assessment: land in sight?
J Am Soc Nephrol. 2011 Jan;22(1):11-3. doi: 10.1681/ASN.2010111132. Epub 2010 Dec 2.
6
Morphometric and visual evaluation of fibrosis in renal biopsies.肾脏活检中纤维化的形态计量学和视觉评估。
J Am Soc Nephrol. 2011 Jan;22(1):176-86. doi: 10.1681/ASN.2009091005. Epub 2010 Nov 29.
7
Prkdc participates in mitochondrial genome maintenance and prevents Adriamycin-induced nephropathy in mice.Prkdc 参与线粒体基因组维护,可预防阿霉素诱导的小鼠肾病。
J Clin Invest. 2010 Nov;120(11):4055-64. doi: 10.1172/JCI43721. Epub 2010 Oct 18.
8
Requirement for class II phosphoinositide 3-kinase C2alpha in maintenance of glomerular structure and function.维持肾小球结构和功能需要 II 类磷酸肌醇 3-激酶 C2α。
Mol Cell Biol. 2011 Jan;31(1):63-80. doi: 10.1128/MCB.00468-10. Epub 2010 Oct 25.
9
Galectin-3 preserves renal tubules and modulates extracellular matrix remodeling in progressive fibrosis.半乳糖凝集素-3 可保护肾小管并调节进行性纤维化中的细胞外基质重塑。
Am J Physiol Renal Physiol. 2011 Jan;300(1):F245-53. doi: 10.1152/ajprenal.00326.2010. Epub 2010 Oct 20.
10
Direct targeting of fibroblast growth factor-inducible 14 protein protects against renal ischemia reperfusion injury.直接靶向成纤维细胞生长因子诱导蛋白 14 可防止肾缺血再灌注损伤。
Kidney Int. 2011 Jan;79(2):179-88. doi: 10.1038/ki.2010.379. Epub 2010 Oct 6.

研究小鼠模型中慢性肾病的发病机制。

Investigating mechanisms of chronic kidney disease in mouse models.

机构信息

Center for Tissue and Cell Sciences, Seattle Children's Research Institute, 1900 Ninth Avenue, M/S C9S-5, Seattle, WA 98101-1309, USA.

出版信息

Pediatr Nephrol. 2012 Aug;27(8):1233-47. doi: 10.1007/s00467-011-1938-2. Epub 2011 Jun 22.

DOI:10.1007/s00467-011-1938-2
PMID:21695449
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3199379/
Abstract

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.

摘要

慢性肾脏病 (CKD) 的动物模型是重要的实验工具,用于在人体临床前测试之前研究新的机制途径并验证潜在的新治疗干预措施。在过去的几年中,小鼠 CKD 模型已被广泛用于这些目的。尽管存在重大局限性,但单侧输尿管梗阻 (UUO) 模型已基本上成为高通量体内模型,因为它在相对较短的时间内再现了所有形式 CKD 的基本发病机制。此外,还可以使用几种替代的小鼠模型来验证新的机制范例和/或新的治疗方法。在这里,我们回顾了几种模型——包括遗传和实验诱导的模型——为研究人员提供了机会,使他们能够将肾脏功能研究终点与纤维化严重程度的定量测量结合起来,而这在 UUO 模型中是不可能的。