Department of Neurology, Neuromuscular Division, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Department of Biological Chemistry and Pharmacology, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Neurobiol Aging. 2021 Aug;104:32-41. doi: 10.1016/j.neurobiolaging.2021.03.005. Epub 2021 Mar 12.
Sarcopenia, or age-related loss of muscle mass and strength, is an important contributor to loss of physical function in older adults. The pathogenesis of sarcopenia is likely multifactorial, but recently the role of neurological degeneration, such as motor unit loss, has received increased attention. Here, we investigated the longitudinal effects of muscle hypertrophy (via overexpression of human follistatin, a myostatin antagonist) on neuromuscular integrity in C57BL/6J mice between the ages of 24 and 27 months. Following follistatin overexpression (delivered via self-complementary adeno-associated virus subtype 9 injection), muscle weight and torque production were significantly improved. Follistatin treatment resulted in improvements of neuromuscular junction innervation and transmission but had no impact on age-related losses of motor units. These studies demonstrate that follistatin overexpression-induced muscle hypertrophy not only increased muscle weight and torque production but also countered age-related degeneration at the neuromuscular junction in mice.
肌肉减少症，或与年龄相关的肌肉质量和力量丧失，是导致老年人身体功能丧失的一个重要因素。肌肉减少症的发病机制可能是多因素的，但最近，神经退行性变的作用，如运动单位的丧失，已受到越来越多的关注。在这里，我们研究了肌肉肥大（通过表达人类卵泡抑素，一种肌肉生长抑制素拮抗剂）对 24 至 27 个月龄 C57BL/6J 小鼠神经肌肉完整性的纵向影响。在卵泡抑素过表达（通过自我互补的腺相关病毒 9 型注射）后，肌肉重量和扭矩产生显著改善。卵泡抑素治疗导致神经肌肉接头神经支配和传递的改善，但对与年龄相关的运动单位丧失没有影响。这些研究表明，卵泡抑素过表达诱导的肌肉肥大不仅增加了肌肉重量和扭矩产生，而且还对抗了小鼠神经肌肉接头的与年龄相关的退化。
