Department of Human Nutrition, Foods, and Exercise and Metabolism Core, Virginia Tech , Blacksburg, Virginia, USA.
Connect Tissue Res. 2021 Jan;62(1):40-52. doi: 10.1080/03008207.2020.1810247. Epub 2020 Aug 31.
To describe potential signaling (cross-talk) between dystrophic skeletal muscle and tendon in Duchenne muscular dystrophy.
Review of Duchenne muscular dystrophy and associated literature relevant to muscle-tendon cross-talk.
Duchenne muscular dystrophy results from the absence of the protein dystrophin and the associated dystrophin - glycoprotein complex, which are thought to provide both structural support and signaling functions for the muscle fiber. In addition, there are other potential signal pathways that could represent cross-talk between muscle and tendon, particularly at the myotendinous junction. Duchenne muscular dystrophy is characterized by multiple pathophysiologic mechanisms. Herein, we explore three of these: (1) the extracellular matrix, fibrosis, and fat deposition; (2) satellite cells; and (3) tensegrity. A key signaling protein that emerged in each was transforming growth factor - beta one (TGF-β1).].
描述杜氏肌营养不良症中营养不良的骨骼肌和肌腱之间的潜在信号(串扰)。
复习杜氏肌营养不良症和与肌肉-肌腱串扰相关的文献。
杜氏肌营养不良症是由于缺乏蛋白肌营养不良和相关的肌营养不良糖蛋白复合物引起的,该复合物被认为为肌纤维提供结构支持和信号功能。此外,还有其他潜在的信号途径可能代表肌肉和肌腱之间的串扰,特别是在肌-腱连接处。杜氏肌营养不良症的特点是多种病理生理机制。在这里,我们探讨其中的三种:(1)细胞外基质、纤维化和脂肪沉积;(2)卫星细胞;和(3)张力整合。每个机制中出现的一个关键信号蛋白是转化生长因子-β1(TGF-β1)。