Nishino I, Fu J, Tanji K, Yamada T, Shimojo S, Koori T, Mora M, Riggs J E, Oh S J, Koga Y, Sue C M, Yamamoto A, Murakami N, Shanske S, Byrne E, Bonilla E, Nonaka I, DiMauro S, Hirano M
Department of Neurology, Columbia University, New York, New York 10032, USA.
Nature. 2000 Aug 24;406(6798):906-10. doi: 10.1038/35022604.
"Lysosomal glycogen storage disease with normal acid maltase" which was originally described by Danon et al., is characterized clinically by cardiomyopathy, myopathy and variable mental retardation. The pathological hallmark of the disease is intracytoplasmic vacuoles containing autophagic material and glycogen in skeletal and cardiac muscle cells. Sarcolemmal proteins and basal lamina are associated with the vacuolar membranes. Here we report ten unrelated patients, including one of the patients from the original case report, who have primary deficiencies of LAMP-2, a principal lysosomal membrane protein. From these results and the finding that LAMP-2-deficient mice manifest a similar vacuolar cardioskeletal myopathy, we conclude that primary LAMP-2 deficiency is the cause of Danon disease. To our knowledge this is the first example of human cardiopathy-myopathy that is caused by mutations in a lysosomal structural protein rather than an enzymatic protein.
最初由达农等人描述的“酸性麦芽糖酶正常的溶酶体糖原贮积病”,临床特征为心肌病、肌病和不同程度的智力发育迟缓。该病的病理特征是骨骼肌和心肌细胞的胞浆内含有自噬物质和糖原的空泡。肌膜蛋白和基膜与空泡膜相关。我们在此报告10例无亲缘关系的患者,包括最初病例报告中的1例患者,他们主要缺乏一种主要的溶酶体膜蛋白LAMP-2。基于这些结果以及LAMP-2缺陷小鼠表现出类似的空泡性心肌骨骼肌病这一发现,我们得出结论,原发性LAMP-2缺乏是达农病的病因。据我们所知,这是人类心肌病-肌病由溶酶体结构蛋白而非酶蛋白突变引起的首个实例。