COPD患者骨骼肌萎缩的分子生物学机制进展

慢性阻塞性肺疾病（COPD）不仅仅是一种局限于呼吸道和肺部的疾病，还是一种可以累及肺外各器官的全身疾病，特别是骨骼肌萎缩和功能障碍，严重影响患者的生活质量及预后。骨骼肌萎缩的机制尚不明确，其机制的发生是多种细胞因子及代谢通路共同参与的复杂过程。目前研究认为自噬、核因子KB、肿瘤坏死因子样弱凋亡诱导因子可能参与了COPD患者骨骼肌萎缩的发生，这些发现可能为COPD防治提供新的策略。

The Molecular Biological Mechanism of Skeletal Muscle Atrophy in COPD Patients

Chronic obstructive pulmonary disease（COPD） is not only a disease limited to the airway and lung, but also a systemic disease involving extrapulmonary organs, especially skeletal muscle atrophy and dys. function,which will se ously impact patients hfe quahty and prognosis. The mechamsm of skeletal muscle atrophy is not clear and the mechanism is a complex process involving a variety of cytokines and metabolic pathways. The present study found that autophagy, nuclear factor KB, and tumor necrosis factor-like weak inducer of apoptosis may be involved in skeletal muscle atrophy in COPD patients, and these findings may provide new strategies for the prevention and treatment of COPD.