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首页> 外文期刊>Veterinary Quarterly >Copper-induced hepatitis: the COMMD1 deficient dog as a translational animal model for human chronic hepatitis
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Copper-induced hepatitis: the COMMD1 deficient dog as a translational animal model for human chronic hepatitis

机译:铜诱发的肝炎:COMMD1缺陷型狗作为人类慢性肝炎的转化动物模型

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Chronic inflammatory liver disease regardless of aetiology leads to failing regeneration and fibrosis, ending in cirrhosis. Both in man and in animals this worldwide health problem has no definitive cure. Chronic liver injury causes hepatic stellate cells to proliferate and differentiate into matrix-producing cells. New therapeutic options will be developed upon detailed understanding of the molecular mechanisms driving liver fibrosis. This may lead to new anti-fibrotic therapies which need to be tested in suitable models before application in the veterinary and human clinic. On the other side, to restore the failing regenerative capacity of the diseased liver cells, adult progenitor cells are of interest, as an alternative to whole organ transplantation. In order to find the most suitable large animal model it is important to recognise that the typical histopathological reaction pattern of the liver can differ between mammalian species. It is therefore imperative that specialists in veterinary internal medicine and pathology, being familiar with the diseases and pathologies of the liver in different animal species, are teaming-up in finding the best models for veterinary and human liver diseases. Several large animal models have been mentioned, like pigs, sheep, and dogs. Based on the observations that man and dog share the same hepatopathies and have identical clinical, pathological and pathogenetic reaction patterns during the development of liver disease, the dog seems to be a properly suited species to test new therapeutic strategies for pets and their best friends.View full textDownload full textKeywordshepatitis, dog, copper, fibrosis, regeneration, Wilson's disease, animal modelRelated var addthis_config = { ui_cobrand: "Taylor & Francis Online", services_compact: "citeulike,netvibes,twitter,technorati,delicious,linkedin,facebook,stumbleupon,digg,google,more", pubid: "ra-4dff56cd6bb1830b" }; var addthis_config = {"data_track_addressbar":true,"ui_click":true}; Add to shortlist Link Permalink http://dx.doi.org/10.1080/01652176.2011.563146
机译:无论病因如何,慢性炎症性肝病都会导致再生和纤维化失败,并最终导致肝硬化。无论是在人类还是动物中,这种全球性的健康问题都无法彻底治愈。慢性肝损伤导致肝星状细胞增殖并分化为产生基质的细胞。在详细了解驱动肝纤维化的分子机制后,将开发出新的治疗选择。这可能会导致需要在兽医和人类诊所中应用之前在合适的模型中进行测试的新抗纤维化疗法。另一方面,为了恢复患病的肝细胞衰竭的再生能力,感兴趣的是成年祖细胞,作为全器官移植的替代方法。为了找到最合适的大型动物模型,重要的是要认识到典型的肝脏组织病理学反应模式在哺乳动物物种之间可能会有所不同。因此,至关重要的是,兽医内部医学和病理学的专家应熟悉不同动物物种肝脏的疾病和病理学,从而联手寻找最佳的兽医和人类肝脏疾病模型。已经提到了几种大型动物模型,例如猪,绵羊和狗。根据观察,人与狗在肝脏疾病的发展过程中有相同的肝病并且具有相同的临床,病理和致病反应模式,因此,该狗似乎是测试宠物及其亲朋好友新治疗策略的合适物种。查看全文下载全文关键词肝炎,狗,铜,纤维化,再生,威尔逊氏病,动物模型相关变量add add_id ,digg,google,more“,发布号:” ra-4dff56cd6bb1830b“}; var addthis_config = {“ data_track_addressbar”:true,“ ui_click”:true};添加到候选列表链接永久链接http://dx.doi.org/10.1080/01652176.2011.563146

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