Gritli-Linde Amel
Department of Oral Biochemistry, Sahlgrenska Academy, University of Gothenburg, Goteborg, Sweden.
Curr Top Dev Biol. 2008;84:37-138. doi: 10.1016/S0070-2153(08)00602-9.
Cleft lip and cleft palate are frequent human congenital malformations with a complex multifactorial etiology. These orofacial clefts can occur as part of a syndrome involving multiple organs or as isolated clefts without other detectable defects. Both forms of clefting constitute a heavy burden to the affected individuals and their next of kin. Human and mouse facial traits are utterly dissimilar. However, embryonic development of the lip and palate are strikingly similar in both species, making the mouse a model of choice to study their normal and abnormal development. Human epidemiological and genetic studies are clearly important for understanding the etiology of lip and palate clefting. However, our current knowledge about the etiopathogenesis of these malformations has mainly been gathered throughout the years from mouse models, including those with mutagen-, teratogen- and targeted mutation-induced clefts as well as from mice with spontaneous clefts. This review provides a comprehensive description of the numerous mouse models for cleft lip and/or cleft palate. Despite a few weak points, these models have revealed a high order of molecular complexity as well as the stringent spatiotemporal regulations and interactions between key factors which govern the development of these orofacial structures.
唇腭裂是常见的人类先天性畸形,病因复杂,涉及多种因素。这些口腔颌面部裂隙可能是涉及多个器官的综合征的一部分,也可能是没有其他可检测到缺陷的孤立性裂隙。这两种形式的腭裂对受影响的个体及其近亲都构成了沉重负担。人类和小鼠的面部特征完全不同。然而,唇和腭的胚胎发育在这两个物种中惊人地相似,这使得小鼠成为研究其正常和异常发育的首选模型。人类流行病学和遗传学研究对于理解唇腭裂的病因显然很重要。然而,多年来我们对这些畸形的发病机制的了解主要来自小鼠模型,包括那些由诱变剂、致畸剂和靶向突变诱导的腭裂模型以及自发腭裂的小鼠模型。本综述全面描述了众多唇裂和/或腭裂小鼠模型。尽管存在一些不足之处,但这些模型揭示了高度的分子复杂性以及关键因素之间严格的时空调节和相互作用,这些因素控制着这些口腔颌面部结构的发育。