慢性阻塞性肺病
转基因小鼠
医学
疾病
转基因
肺病
发病机制
基因
基因靶向
免疫学
生物信息学
计算生物学
病理
生物
遗传学
内科学
出处
期刊:The European respiratory journal
[European Respiratory Society]
日期:2007-01-30
卷期号:29 (2): 375-378
被引量:58
标识
DOI:10.1183/09031936.00087606
摘要
Animal models play an important role in the understanding of the pathogenesis of chronic obstructive pulmonary disease (COPD). The applicability of findings to human COPD depends upon several factors, including the disease model, and similarities in mouse structure and function between species. There are many examples in the literature of transgenic mice that have contributed to the understanding of COPD. Several studies demonstrate the complexity of inflammatory networks and how unexpected findings in animal models have led to the search for new potential mediators in human disease. Gene-targeting studies into α 1 -antitrypsin (α 1 -AT) and emphysema in mice have demonstrated that the genetic locus for α 1 -AT in mice is very complex and that the loss of one gene is lethal in embryo lung development. This underlines the differences between mice and humans that limit the ability to translate between systems in some instances. Gene targeting has also highlighted complex roles for transforming growth factor-β in COPD and has been used to determine important molecules and pathways in COPD. Both transgenic and gene-targeted models suffer limitations and their applicability to human chronic obstructive pulmonary disease may be dependant on several factors, some of which are still being learnt. The more that is known about similarities and differences, the better the knowledge will be that is gained to develop for chronic obstructive pulmonary disease.
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