Bushby K M
Department of Biochemistry and Genetics, University of Newcastle-upon-Tyne, UK.
Brain. 1999 Aug;122 ( Pt 8):1403-20. doi: 10.1093/brain/122.8.1403.
The clinical heterogeneity which has long been recognized in the limb-girdle muscular dystrophies (LGMD) has been shown to relate to the involvement of a large number of different genes. At least eight forms of autosomal recessive LGMD and three forms of autosomal dominant disease are now recognized and can be defined by the primary gene or protein involved, or by a genetic localization. These advances have combined the approaches of positional cloning and candidate gene analysis to great effect, with the pivotal role of the dystrophin-associated complex confirmed through the involvement of at least four dystrophin-associated proteins in different subtypes of autosomal recessive LGMD (the sarcoglycanopathies). Two novel mechanisms may have to be postulated to explain the involvement of the calpain 3 and dysferlin genes in other forms of LGMD. Using the diagnostic tools which have become available as a result of this increased understanding, the clinical features of the various subtypes are also becoming clearer, with useful diagnostic and prognostic information at last available to the practising clinician.
长期以来,人们认识到肢带型肌营养不良症(LGMD)存在临床异质性,现已证明这与大量不同基因的参与有关。目前已确认至少有八种常染色体隐性LGMD形式和三种常染色体显性疾病形式,可通过所涉及的主要基因或蛋白质,或通过基因定位来定义。这些进展极大地结合了定位克隆和候选基因分析方法,通过至少四种抗肌萎缩蛋白相关蛋白参与常染色体隐性LGMD的不同亚型(肌聚糖病),证实了抗肌萎缩蛋白相关复合物的关键作用。可能必须假定两种新机制来解释钙蛋白酶3和dysferlin基因在其他形式LGMD中的参与情况。利用由于这种深入了解而获得的诊断工具,各种亚型的临床特征也越来越清晰,终于为临床医生提供了有用的诊断和预后信息。