Castro-Gago Manuel, Blanco-Barca Manuel O, Eiris-Puñal Jesús, Carneiro Isabel, Arce Victor M, Devesa Jesús
Departamento de Pediatría, Servicio de Neuropediatría, Hospital Clínico Universitario, Santiago de Compostela, Spain.
Pediatr Neurol. 2006 Apr;34(4):281-4. doi: 10.1016/j.pediatrneurol.2005.08.009.
The demonstration that myostatin may negatively regulate muscle mass in adult individuals has raised the possibility of targeting the myostatin pathway in order to increase muscle growth in a variety of muscle degenerative and wasting conditions. In this regard, blockade of endogenous myostatin results in anatomic, biochemical, and physiologic improvement in the dystrophic phenotype in the mdx mouse. Moreover, myostatin messenger ribonucleic acid levels are decreased in the regenerated muscle of these mice, suggesting that myostatin may also be involved in the pathogenesis of the disease. To gain further insight into the possible role of myostatin in muscle degenerative diseases, the present work investigates the expression of muscle myostatin in children with muscular dystrophies and mitochondrial encephalomyopathies. No differences in the pattern of myostatin expression were evident in any case, even in those patients with prominent muscular atrophy. These findings suggest that muscle loss that can be observed in muscle degenerative diseases does not depend on changes in myostatin expression.
证明肌生成抑制素可能对成年个体的肌肉质量产生负调节作用,这引发了针对肌生成抑制素途径以在各种肌肉退行性和萎缩性病症中促进肌肉生长的可能性。在这方面,内源性肌生成抑制素的阻断导致mdx小鼠营养不良表型在解剖学、生物化学和生理学上得到改善。此外,这些小鼠再生肌肉中的肌生成抑制素信使核糖核酸水平降低,表明肌生成抑制素可能也参与了该疾病的发病机制。为了进一步深入了解肌生成抑制素在肌肉退行性疾病中的可能作用,本研究调查了患有肌肉营养不良症和线粒体脑肌病的儿童肌肉中肌生成抑制素的表达情况。在任何情况下,即使是那些有明显肌肉萎缩的患者,肌生成抑制素表达模式均无明显差异。这些发现表明,在肌肉退行性疾病中观察到的肌肉损失并不取决于肌生成抑制素表达的变化。