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阿霉素肾病:局灶节段性肾小球硬化模型。

Adriamycin nephropathy: a model of focal segmental glomerulosclerosis.

机构信息

Centre for Transplant and Renal Research, Westmead Millennium Institute, University of Sydney at Westmead Hospital, Sydney, New South Wales, Australia.

出版信息

Nephrology (Carlton). 2011 Jan;16(1):30-8. doi: 10.1111/j.1440-1797.2010.01383.x.

DOI:10.1111/j.1440-1797.2010.01383.x
PMID:21175974
Abstract

Adriamycin nephropathy (AN) is a rodent model of chronic kidney disease that has been studied extensively and has enabled a greater understanding of the processes underlying the progression of chronic proteinuric renal disease. AN is characterized by podocyte injury followed by glomerulosclerosis, tubulointerstitial inflammation and fibrosis. Genetic studies have demonstrated a number of loci that alter both risk and severity of renal injury induced by Adriamycin. Adriamycin-induced renal injury has been shown in numerous studies to be modulated by both non-immune and immune factors, and has facilitated further study of mechanisms of tubulointerstitial injury. This review will outline the pharmacological behaviour of Adriamycin, and describe in detail the model of AN, including its key structural characteristics, genetic susceptibility and pathogenesis.

摘要

阿霉素肾病(AN)是一种慢性肾病的啮齿动物模型,已经得到了广泛的研究,使人们对慢性蛋白尿性肾病进展的过程有了更深入的了解。AN 的特征是足细胞损伤,随后发生肾小球硬化、肾小管间质炎症和纤维化。遗传研究已经证实了一些改变阿霉素诱导的肾脏损伤风险和严重程度的基因座。大量研究表明,阿霉素诱导的肾损伤可被非免疫和免疫因素调节,并促进了对肾小管间质损伤机制的进一步研究。这篇综述将概述阿霉素的药理学行为,并详细描述 AN 模型,包括其关键结构特征、遗传易感性和发病机制。

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Adriamycin nephropathy: a model of focal segmental glomerulosclerosis.阿霉素肾病:局灶节段性肾小球硬化模型。
Nephrology (Carlton). 2011 Jan;16(1):30-8. doi: 10.1111/j.1440-1797.2010.01383.x.
2
Passive Heymann nephritis: evidence that angiotensin-converting enzyme inhibition reduces proteinuria and retards renal structural injury.被动型海曼肾炎:血管紧张素转换酶抑制可减少蛋白尿并延缓肾脏结构损伤的证据
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C5b-9 regulates peritubular myofibroblast accumulation in experimental focal segmental glomerulosclerosis.C5b-9在实验性局灶节段性肾小球硬化中调节肾小管周肌成纤维细胞的积聚。
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Glomerular hypertrophy and epithelial cell injury modulate progressive glomerulosclerosis in the rat.肾小球肥大和上皮细胞损伤调节大鼠进行性肾小球硬化。
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Rapamycin attenuates the severity of murine adriamycin nephropathy.雷帕霉素减轻小鼠阿霉素肾病的严重程度。
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Glomerulosclerosis 4 weeks after administration of adriamycin in a single dose.单次给予阿霉素4周后的肾小球硬化。
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A protective role for programmed death 1 in progression of murine adriamycin nephropathy.程序性死亡蛋白1在小鼠阿霉素肾病进展中的保护作用。
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Osteopontin as an injury marker expressing in epithelial hyperplasia lesions helpful in prognosis of focal segmental glomerulosclerosis.骨桥蛋白作为一种在上皮增生性病变中表达的损伤标志物,有助于局灶节段性肾小球硬化的预后判断。
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Animal models of FSGS: lessons for pathogenesis and treatment.局灶节段性肾小球硬化的动物模型:对发病机制和治疗的启示
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The alternative pathway of complement is activated in the glomeruli and tubulointerstitium of mice with adriamycin nephropathy.在阿霉素肾病小鼠的肾小球和肾小管间质中,补体替代途径被激活。
Am J Physiol Renal Physiol. 2007 Aug;293(2):F555-64. doi: 10.1152/ajprenal.00403.2006. Epub 2007 May 23.

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