Anderson J E, Liu L, Kardami E
Department of Anatomy, University of Manitoba, Winnipeg, Canada.
Muscle Nerve. 1994 Jan;17(1):64-73. doi: 10.1002/mus.880170109.
Muscle damage and repair were studied in mdx mice treated with triiodothyronine (T3) for 14 days. Hindlimb and cardiac muscles were examined for the severity of dystrophy, the degree of muscle centronucleation, and fiber size. In control and mdx mice, cardiac hypertrophy and skeletal muscle atrophy were present after T3 treatment. Both cardiac and soleus (but not fast-twitch) muscles had larger, more frequent dystrophic lesions in T3-treated mdx mice, and mdx soleus had an increased area of new myotubes after T3. Skeletal myogenesis in mdx mice may have been delayed by excess T3, possibly related to the general reduction in staining for basic fibroblast growth factor in hyperthyroid mice. These are the first observations of a metabolic perturbation which worsens mdx dystrophy and possibly repair in a muscle-specific manner, and are likely related to T3-induced changes in myosin heavy chain expression, and to increased mechanical strain on dystrophin-deficient muscles.
研究了用三碘甲状腺原氨酸（T3）治疗14天的mdx小鼠的肌肉损伤和修复情况。检查了后肢和心肌的营养不良严重程度、肌肉中心核化程度以及纤维大小。在对照和mdx小鼠中，T3治疗后出现心脏肥大和骨骼肌萎缩。在T3治疗的mdx小鼠中，心肌和比目鱼肌（但不是快肌）都有更大、更频繁的营养不良性病变，并且mdx比目鱼肌在T3治疗后新肌管面积增加。mdx小鼠的骨骼肌生成可能因过量T3而延迟，这可能与甲状腺功能亢进小鼠中碱性成纤维细胞生长因子染色的普遍减少有关。这些是首次观察到的一种代谢紊乱，它会使mdx营养不良恶化，并可能以肌肉特异性方式进行修复，这可能与T3诱导的肌球蛋白重链表达变化以及肌营养不良蛋白缺陷肌肉上机械应变增加有关。
