Suzuki K, Proia R L, Suzuki K
Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill 27599-7525, USA.
Brain Pathol. 1998 Jan;8(1):195-215. doi: 10.1111/j.1750-3639.1998.tb00145.x.
Genetically authentic animal models of human lysosomal diseases occur spontaneously in many mammalian species. However, most are among larger domestic or farm animals with only two well-defined genetic lysosomal diseases known among rodents. This status changed dramatically in recent years with the advent of the combined homologous recombination and embryonic stem cell technology, which allows directed generation of mouse models that are genetically equivalent to human diseases. Almost all known human sphingolipidoses, two mucopolysaccharidoses and aspartylglycosaminuria have so far been duplicated in mice and more are expected in the near future. This technology also allows generation of mouse mutants that are not known or are highly unlikely to exist in humans, such as "double-knockouts." These animal models will play an important role in studies of the pathogenesis and treatment of these disorders. While the utility of these mouse models is obvious, species differences in brain development and metabolic pathways must be always remembered, if the ultimate goal of the study is application to human patients.
人类溶酶体疾病的基因纯正动物模型在许多哺乳动物物种中自发出现。然而,大多数存在于较大的家畜或农场动物中,啮齿动物中仅已知两种明确的遗传性溶酶体疾病。近年来,随着同源重组和胚胎干细胞技术的结合,这种情况发生了巨大变化,该技术允许直接生成与人类疾病基因等效的小鼠模型。迄今为止,几乎所有已知的人类鞘脂贮积症、两种粘多糖贮积症和天冬氨酰葡糖胺尿症都已在小鼠中复制,预计在不久的将来还会有更多。这项技术还允许生成在人类中未知或极不可能存在的小鼠突变体,如“双敲除”。这些动物模型将在这些疾病的发病机制和治疗研究中发挥重要作用。虽然这些小鼠模型的实用性显而易见,但如果研究的最终目标是应用于人类患者,必须始终牢记大脑发育和代谢途径中的物种差异。