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本文引用的文献

1
Defective glucose metabolism in polycystic kidney disease identifies a new therapeutic strategy.多囊肾病中葡萄糖代谢缺陷为新的治疗策略提供了依据。
Nat Med. 2013 Apr;19(4):488-93. doi: 10.1038/nm.3092. Epub 2013 Mar 24.
2
Network analysis of a Pkd1-mouse model of autosomal dominant polycystic kidney disease identifies HNF4α as a disease modifier.常染色体显性多囊肾病 Pkd1 小鼠模型的网络分析确定 HNF4α 为疾病修饰因子。
PLoS Genet. 2012;8(11):e1003053. doi: 10.1371/journal.pgen.1003053. Epub 2012 Nov 29.
3
Pasireotide is more effective than octreotide in reducing hepatorenal cystogenesis in rodents with polycystic kidney and liver diseases.培高利特在减少多囊肾病和肝病啮齿动物的肝肾功能囊肿形成方面比奥曲肽更有效。
Hepatology. 2013 Jul;58(1):409-21. doi: 10.1002/hep.26140. Epub 2013 Mar 6.
4
Model organisms: There's more to life than rats and flies.模式生物:生命不仅仅只有大鼠和果蝇。
Nature. 2012 Nov 1;491(7422):31-3. doi: 10.1038/491031a.
5
Tolvaptan in patients with autosomal dominant polycystic kidney disease.托伐普坦治疗常染色体显性遗传多囊肾病。
N Engl J Med. 2012 Dec 20;367(25):2407-18. doi: 10.1056/NEJMoa1205511. Epub 2012 Nov 3.
6
Functional polycystin-1 dosage governs autosomal dominant polycystic kidney disease severity.多囊蛋白-1 的功能剂量决定常染色体显性遗传多囊肾病的严重程度。
J Clin Invest. 2012 Nov;122(11):4257-73. doi: 10.1172/JCI64313. Epub 2012 Oct 15.
7
Cilia at the node of mouse embryos sense fluid flow for left-right determination via Pkd2.小鼠胚胎节点处的纤毛通过 Pkd2 感受流体流动以进行左右确定。
Science. 2012 Oct 12;338(6104):226-31. doi: 10.1126/science.1222538. Epub 2012 Sep 13.
8
The mammalian gene function resource: the International Knockout Mouse Consortium.哺乳动物基因功能资源:国际基因敲除小鼠联盟。
Mamm Genome. 2012 Oct;23(9-10):580-6. doi: 10.1007/s00335-012-9422-2. Epub 2012 Sep 12.
9
Gene editing: not just for translation anymore.基因编辑:不再仅仅用于翻译了。
Nat Methods. 2011 Dec 28;9(1):28-31. doi: 10.1038/nmeth.1811.
10
The APL paradigm and the "co-clinical trial" project.APL 范式与“共临床试验”项目。
Cancer Discov. 2011 Jul;1(2):108-16. doi: 10.1158/2159-8290.CD-11-0061.

多囊肾病的小鼠模型

Murine Models of Polycystic Kidney Disease.

作者信息

Menezes Luis Fernando, Germino Gregory George

机构信息

Kidney Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 10 Room 8D46, 10 Center Drive, Bethesda, MD 20892.

出版信息

Drug Discov Today Dis Mech. 2013 Dec 1;10(3-4):e153-e158. doi: 10.1016/j.ddmec.2013.10.002.

DOI:10.1016/j.ddmec.2013.10.002
PMID:25013443
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4085131/
Abstract

Polycystic diseases affect approximately 1/1000 and are important causes of kidney failure. No therapies presently are in clinical practice that can prevent disease progression. Multiple mouse models have been produced for the genetic forms of the disease that most commonly affect humans. In this report, we review recent progress in the field and describe some of the outstanding challenges.

摘要

多囊性疾病影响约千分之一的人群,是肾衰竭的重要病因。目前尚无临床实践中可用于预防疾病进展的疗法。针对最常影响人类的该疾病遗传形式,已构建了多种小鼠模型。在本报告中,我们回顾了该领域的最新进展并描述了一些突出的挑战。