Department of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
Brain Pathol. 2012 Jan;22(1):82-8. doi: 10.1111/j.1750-3639.2011.00543.x.
Lysosomal myopathies are hereditary myopathies characterized morphologically by the presence of autophagic vacuoles. In mammals, autophagy plays an important role for the turnover of cellular components, particularly in response to starvation or glucagons. In normal muscle, autolysosomes or autophagosomes are typically inconspicuous. In distinct neuromuscular disorders, however, lysosomes become structurally abnormal and functionally impaired, leading to the accumulation of autophagic vacuoles in myofibers. In some instances, the accumulation of autophagic vacuoles can be a prominent feature, implicating autophagy as a contributor to disease pathomechanism and/or progression. At present, there are two disorders in the muscle that are associated with a primary defect in lysosomal proteins, namely Pompe disease and Danon disease. This review will give a brief discussion on these disorders, highlighting the role of autophagy in disease progression.
溶酶体肌病是一种遗传性肌病,其形态学特征为自噬小体的存在。在哺乳动物中,自噬对于细胞成分的更新起着重要作用,特别是在饥饿或胰高血糖素的刺激下。在正常肌肉中,自溶体或自噬体通常不明显。然而,在某些神经肌肉疾病中,溶酶体的结构变得异常,功能受损,导致肌纤维中自噬小体的积累。在某些情况下,自噬小体的积累可能是一个显著特征,表明自噬是疾病发病机制和/或进展的一个因素。目前,有两种肌肉疾病与溶酶体蛋白的主要缺陷有关,即庞贝病和丹顿病。这篇综述将简要讨论这些疾病,强调自噬在疾病进展中的作用。