Rodent models of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.
Rodent models of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.
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DOI：
10.3390/ijms141121833
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发表时间：
2013-11-04
影响因子：
5.6
通讯作者：
Nakajima A
中科院分区：
文献类型：
--
作者：
Imajo K;Yoneda M;Kessoku T;Ogawa Y;Maeda S;Sumida Y;Hyogo H;Eguchi Y;Wada K;Nakajima A
非酒精性脂肪性肝病（NAFLD），包括非酒精性脂肪性肝炎（NASH）的研究，由于该疾病合适模型的可用性而受到限制。已经描述了许多啮齿动物模型，其中相关的肝脏病理学在适当的代谢背景下发展。这些模型对于研究 NASH 关键问题之一的研究人员来说是很有前途的工具：与其说脂肪变性发生的原因，不如说是什么导致从简单的脂肪变性转变为脂肪性肝炎的炎症性、进行性纤维化状况。不同的啮齿动物模型可以分为两大类。第一种是通过饮食或药物操作获得疾病的模型，第二种是转基因模型，其中肝脏疾病自发发展。迄今为止，还没有单一的啮齿动物模型能够涵盖人类疾病进展的全部范围，但单个模型可以模仿人类疾病的特定特征。因此，研究人员选择合适的啮齿动物模型非常重要。本综述的目的是讨论目前可用的 NAFLD 啮齿动物模型中存在的代谢异常，总结已建立模型的优点和缺点以及加深我们对该疾病发病机制了解的关键发现。
Research in nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH), has been limited by the availability of suitable models for this disease. A number of rodent models have been described in which the relevant liver pathology develops in an appropriate metabolic context. These models are promising tools for researchers investigating one of the key issues of NASH: not so much why steatosis occurs, but what causes the transition from simple steatosis to the inflammatory, progressive fibrosing condition of steatohepatitis. The different rodent models can be classified into two large groups. The first includes models in which the disease is acquired after dietary or pharmacological manipulation, and the second, genetically modified models in which liver disease develops spontaneously. To date, no single rodent model has encompassed the full spectrum of human disease progression, but individual models can imitate particular characteristics of human disease. Therefore, it is important that researchers choose the appropriate rodent models. The purpose of the present review is to discuss the metabolic abnormalities present in the currently available rodent models of NAFLD, summarizing the strengths and weaknesses of the established models and the key findings that have furthered our understanding of the disease’s pathogenesis.
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影响因子：
4.2
作者：
Bennett, M. J.
通讯作者：
Bennett, M. J.
DOI：
10.1016/j.bbrc.2006.02.032
发表时间：
2006-04-21
影响因子：
3.1
作者：
Arsov, T;Larter, CZ;Farrell, GC
通讯作者：
Farrell, GC
影响因子：
4.8
作者：
Alb, JG;Cortese, JD;Bankaitis, VA
通讯作者：
Bankaitis, VA
影响因子：
3.2
作者：
Day, CP
通讯作者：
Day, CP
影响因子：
4.8
作者：
Fan, CY;Pan, J;Reddy, JK
通讯作者：
Reddy, JK