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本文引用的文献

1
The kd/kd mouse is a model of collapsing glomerulopathy.kd/kd小鼠是局灶节段性肾小球硬化症的一种模型。
J Am Soc Nephrol. 2005 Oct;16(10):2847-51. doi: 10.1681/ASN.2005050494. Epub 2005 Aug 24.
2
Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis.肠道稳态需要Toll样受体识别共生微生物群。
Cell. 2004 Jul 23;118(2):229-41. doi: 10.1016/j.cell.2004.07.002.
3
Mutant prenyltransferase-like mitochondrial protein (PLMP) and mitochondrial abnormalities in kd/kd mice.kd/kd小鼠中的突变型类异戊二烯基转移酶线粒体蛋白(PLMP)与线粒体异常
Kidney Int. 2004 Jul;66(1):20-8. doi: 10.1111/j.1523-1755.2004.00702.x.
4
An abundance of Escherichia coli is harbored by the mucosa-associated bacterial flora of interleukin-2-deficient mice.白细胞介素-2缺陷小鼠的黏膜相关细菌菌群中存在大量大肠杆菌。
Infect Immun. 2004 Apr;72(4):1983-90. doi: 10.1128/IAI.72.4.1983-1990.2004.
5
Signaling danger: toll-like receptors and their potential roles in kidney disease.信号传递危险:Toll样受体及其在肾脏疾病中的潜在作用。
J Am Soc Nephrol. 2004 Apr;15(4):854-67. doi: 10.1097/01.asn.0000121781.89599.16.
6
Cutting Edge: Multiple autoimmune pathways in kd/kd mice.前沿:kd/kd小鼠中的多种自身免疫途径。
J Immunol. 2003 Sep 15;171(6):2778-81. doi: 10.4049/jimmunol.171.6.2778.
7
Influence of aging and long-term caloric restriction on oxygen radical generation and oxidative DNA damage in rat liver mitochondria.衰老和长期热量限制对大鼠肝脏线粒体氧自由基生成及氧化性DNA损伤的影响。
Free Radic Biol Med. 2002 May 1;32(9):882-9. doi: 10.1016/s0891-5849(02)00773-6.
8
Toll-like receptors: key mediators of microbe detection.Toll样受体:微生物检测的关键介质。
Curr Opin Immunol. 2002 Feb;14(1):103-10. doi: 10.1016/s0952-7915(01)00304-1.
9
Caloric restriction decreases mitochondrial free radical generation at complex I and lowers oxidative damage to mitochondrial DNA in the rat heart.热量限制可减少大鼠心脏中复合体 I 处的线粒体自由基生成,并降低对线粒体 DNA 的氧化损伤。
FASEB J. 2001 Jul;15(9):1589-91. doi: 10.1096/fj.00-0764fje.
10
Localization of the mouse kidney disease (kd) gene to a YAC/BAC contig on Chromosome 10.小鼠肾病(kd)基因在10号染色体上的YAC/BAC重叠群中的定位。
Mamm Genome. 2000 Nov;11(11):967-71. doi: 10.1007/s003350010188.

无菌条件下kd/kd小鼠的线粒体和肾脏疾病表型。

The mitochondrial and kidney disease phenotypes of kd/kd mice under germfree conditions.

作者信息

Hallman Troy M, Peng Min, Meade Ray, Hancock Wayne W, Madaio Michael P, Gasser David L

机构信息

University Laboratory Animal Resources, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

出版信息

J Autoimmun. 2006 Feb;26(1):1-6. doi: 10.1016/j.jaut.2005.10.006. Epub 2005 Dec 6.

DOI:10.1016/j.jaut.2005.10.006
PMID:16337774
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2254222/
Abstract

Interstitial nephritis occurs spontaneously in kd/kd mice, but the mechanisms leading to this disease have not been fully elucidated. The earliest manifestation of a phenotype is the appearance of ultrastructural defects in the mitochondria of mice as young as 42 days of age. To examine the influence of the environment on the phenotype, homozygous B6.kd/kd mice were transferred from specific pathogen-free (SPF) conditions to a germfree (GF) environment, and the development of the disease was observed. The GF state resulted in a highly significant reduction in the frequency of tubulointerstitial nephritis. In addition, GF conditions markedly reduced the appearance of the mitochondrial phenotype, with no sign of mitochondrial abnormalities in GF mice of up to 155 days of age. These results suggest that environmental factors are involved in the progression of all known manifestations of this disease phenotype.

摘要

间质性肾炎在kd/kd小鼠中自发发生,但导致这种疾病的机制尚未完全阐明。最早的表型表现是在年仅42天的小鼠线粒体中出现超微结构缺陷。为了研究环境对表型的影响,将纯合B6.kd/kd小鼠从无特定病原体(SPF)条件转移到无菌(GF)环境中,并观察疾病的发展情况。无菌状态导致肾小管间质性肾炎的发生率显著降低。此外,无菌条件显著减少了线粒体表型的出现,在长达155天的无菌小鼠中没有线粒体异常的迹象。这些结果表明,环境因素参与了这种疾病表型所有已知表现的进展。