梅斯医学MedSci APP
医路相伴，成就大医
梅斯医学MedSci APP
医路相伴，成就大医
2012年10月17日目前治疗肌肉损伤的药物很少，肌萎缩和家族性遗传病可以引发肌肉变性，比如迪谢纳肌营养不良症。近日，一项研究发现或许帮助医生们治疗这种肌肉疾病，相关研究由渥太华大学医学院等处的研究者进行，研究成果刊登于10月16日的国际杂志Science Signaling上。
研究者Korneluk教授表示，我们都知道，目前很多制药公司都在积极推进抗癌药物的研发和临床试验，这些抗癌药物都以IAP基因为靶点，IAP基因所编码的蛋白质是和肿瘤生长相关的一个蛋白质家族。如今研究者将IAP基因的角色同肌肉疾病联系了起来，研究者发现以IAP为靶点的药物可以促进癌症细胞死亡，于此同时可以诱导和修复肌肉组织。研究者也通过激活特殊的信号交流路径来鉴别出了这一过程发生的分子机制。这项路径通过促进肌肉细胞融合形成新的肌肉纤维来修复肌肉组织，从而达到控制肌肉生长以及修复的作用。
演技足额和希望在未来通过进行相应的临床试验来验证其结果，研究小组同时也发现了一些肌肉增强效应的药物可以重复作为一种生长因子在机体进行作用，称为TWEAK。当其水平较低时，相同的信号路径就会被激活，从而促进损伤肌肉组织的修复。
这项研究由加拿大卫生研究院等机构提供支持。
与肌肉相关的拓展阅读：
TWEAK and cIAP1 Regulate Myoblast Fusion Through the Noncanonical NF-B Signaling Pathway
The fusion of mononucleated muscle progenitor cells (myoblasts) into multinucleated muscle fibers is a critical aspect of muscle development and regeneration. We identified the noncanonical nuclear factor B (NF-B) pathway as a signaling axis that drives the recruitment of myoblasts into new muscle fibers. Loss of cellular inhibitor of apoptosis 1 (cIAP1) protein led to constitutive activation of the noncanonical NF-B pathway and an increase in the number of nuclei per myotube. Knockdown of essential mediators of NF-B signaling, such as p100, RelB, inhibitor of B kinase α, and NF-B–inducing kinase, attenuated myoblast fusion in wild-type myoblasts. In contrast, the extent of myoblast fusion was increased when the activity of the noncanonical NF-B pathway was enhanced by increasing the abundance of p52 and RelB or decreasing the abundance of tumor necrosis factor (TNF) receptor–associated factor 3, an inhibitor of this pathway. Low concentrations of the cytokine TNF-like weak inducer of apoptosis (TWEAK), which preferentially activates the noncanonical NF-B pathway, also increased myoblast fusion, without causing atrophy or impairing myogenesis. These results identify roles for TWEAK, cIAP1, and noncanonical NF-B signaling in the regulation of myoblast fusion and highlight a role for cytokine signaling during adult skeletal myogenesis.
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