The escalation of life expectancy is accompanied by an increase in the prevalence of age-related conditions, such as sarcopenia. Sarcopenia, a muscle condition defined by low muscle strength, muscle quality or quantity, and physical performance, has a high prevalence among the elderly and is associated to increased mortality. The neuromuscular system has been emerging as a key contributor to sarcopenia pathogenesis. Indeed, the age-related degeneration of the neuromuscular junction (NMJ) function and structure may contribute to the loss of muscle strength and ultimately to the loss of muscle mass that characterize sarcopenia. The present mini-review discusses important signaling pathways involved in the function and maintenance of the NMJ, giving emphasis to the ones that might contribute to sarcopenia pathogenesis. Some conceivable biomarkers, such as C-terminal agrin fragment (CAF) and brain-derived neurotrophic factor (BDNF), and therapeutic targets, namely acetylcholine and calcitonin gene–related peptide (CGRP), can be retrieved, making way to future studies to validate their clinical use.

预期寿命的延长伴随着年龄相关疾病的患病率增加，例如肌肉减少症。肌肉减少症是一种由肌肉力量、肌肉质量或数量以及身体机能低下定义的肌肉状况，在老年人中的患病率很高，并且与死亡率增加有关。神经肌肉系统已成为肌肉减少症发病机制的关键因素。事实上，与年龄相关的神经肌肉接头 (NMJ) 功能和结构的退化可能会导致肌肉力量的丧失，并最终导致肌肉减少症的肌肉质量下降。本小型综述讨论了与 NMJ 的功能和维持有关的重要信号通路，并强调了可能导致肌肉减少症发病机制的信号通路。一些可以想象的生物标志物，