Stauber W T, Fritz V K, Clarkson P M, Riggs J E
Department of Physiology, West Virginia University, Morgantown 26506.
Med Hypotheses. 1991 Aug;35(4):358-62. doi: 10.1016/0306-9877(91)90285-7.
The pathogenesis of dystrophin deficient myopathies remains unknown. Rat and human muscles subjected to severe injury following repeated eccentric muscle actions demonstrate histopathological alterations which mimic a dystrophic process. Immunofluorescent histochemical examination of these injured muscles demonstrates a separation of proteoglycans of the basal lamina from the muscle plasma membrane, the identical histopathological alteration observed in Duchenne muscular dystrophy. These findings are consistent with the hypothesis that dystrophin is essential for maintenance of the structural integrity of the sarcolemma.
抗肌萎缩蛋白缺乏性肌病的发病机制尚不清楚。大鼠和人类的肌肉在反复进行离心肌肉运动后受到严重损伤，表现出模仿营养不良过程的组织病理学改变。对这些受损肌肉进行免疫荧光组织化学检查发现，基底膜的蛋白聚糖与肌细胞膜分离，这与杜兴氏肌营养不良症中观察到的相同组织病理学改变。这些发现与抗肌萎缩蛋白对维持肌膜结构完整性至关重要的假说一致。
