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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

Animal models of FSGS: lessons for pathogenesis and treatment.

作者信息

Fogo Agnes B

机构信息

Department of Pathology, Vanderbilt University Medical Center, Nashville, TN, USA.

出版信息

Semin Nephrol. 2003 Mar;23(2):161-71. doi: 10.1053/snep.2003.50015.

Abstract

Glomerulosclerosis in a heterogeneous pattern, ie, focal and segmental glomerulosclerosis (FSGS), is a common endpoint in a variety of settings, including idiopathic FSGS, and scarring secondary to other renal or systemic diseases. These different causes contribute to the diverse clinical outcomes of histological focal sclerosis, and the varying histologic manifestations of sclerosis. Numerous models have been established in the rat that aim to mirror the various elements of human glomerulosclerosis. With the availability of knockout gene technology, many, but not all of these models have been translated to mouse species. This review will focus on the remnant kidney model, the podocyte injury models of puromycin aminonucleoside or adriamycin injection, and examples of newly developed genetic models, such as knockout of CD2 associated protein (CD2AP).

摘要

异质性模式的肾小球硬化,即局灶节段性肾小球硬化(FSGS),是多种情况下的常见终点,包括特发性FSGS以及继发于其他肾脏或全身性疾病的瘢痕形成。这些不同病因导致了组织学局灶性硬化的不同临床结局以及硬化的不同组织学表现。在大鼠中已经建立了许多旨在反映人类肾小球硬化各种要素的模型。随着基因敲除技术的出现,其中许多(但并非全部)模型已转化为小鼠模型。本综述将重点关注残余肾模型、嘌呤霉素氨基核苷或阿霉素注射的足细胞损伤模型以及新开发的遗传模型实例,如CD2相关蛋白(CD2AP)基因敲除模型。

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