ELEGI Laboratory, Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK.
Curr Opin Pulm Med. 2010 Mar;16(2):123-33. doi: 10.1097/MCP.0b013e328336438d.
The purpose of this review is to identify new advances in our understanding of skeletal muscle dysfunction in patients with chronic obstructive pulmonary disease (COPD).
Recent studies have confirmed the relevance of muscle dysfunction as an independent prognosis factor in COPD. Animal studies have shed light on the molecular mechanisms governing skeletal muscle hypertrophy/atrophy. Recent evidence in patients with COPD highlighted the contribution of protein breakdown and mitochondrial dysfunction as pathogenic mechanisms leading to muscle dysfunction in these patients.
COPD is a debilitating disease impacting negatively on health status and the functional capacity of patients. COPD goes beyond the lungs and incurs significant systemic effects among which muscle dysfunction/wasting is one of the most important. Muscle dysfunction is a prominent contributor to exercise limitation, healthcare utilization and an independent predictor of morbidity and mortality. Gaining more insight into the molecular mechanisms leading to muscle dysfunction/wasting is key for the development of new and tailored therapeutic strategies to tackle skeletal muscle dysfunction/wasting in COPD patients.
本综述旨在确定慢性阻塞性肺疾病（COPD）患者骨骼肌功能障碍认识方面的新进展。
近期研究证实了肌肉功能障碍作为 COPD 独立预后因素的相关性。动物研究揭示了调控骨骼肌肥大/萎缩的分子机制。近期 COPD 患者的证据强调了蛋白分解和线粒体功能障碍作为导致这些患者肌肉功能障碍的发病机制的重要性。
COPD 是一种使人虚弱的疾病，对健康状况和患者的功能能力产生负面影响。COPD 不仅影响肺部，还会导致全身性的显著影响，其中肌肉功能障碍/损耗是最重要的影响之一。肌肉功能障碍是导致运动受限、医疗保健利用增加的主要因素，也是发病率和死亡率的独立预测因素。深入了解导致肌肉功能障碍/损耗的分子机制，对于开发新的、有针对性的治疗策略来解决 COPD 患者的骨骼肌功能障碍/损耗至关重要。
