State Key Lab of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical College, Guangdong 510012, China.
Respir Med. 2012 Jan;106(1):102-8. doi: 10.1016/j.rmed.2011.07.016. Epub 2011 Aug 15.
It is well confirmed that myostatin is a negative regulator of skeletal muscle mass and implicated in several diseases involved in muscle wasting and cachexia. Skeletal muscle wasting is an important systemic manifestation of chronic obstructive pulmonary disease (COPD), while the expression of circulating myostatin in COPD remains unclear. The aim of this study was to investigate the expression of circulating myostatin and its relationship with skeletal muscle wasting in COPD.
Seventy-one patients with stable COPD and sixty age-matched, healthy control subjects participated in the study. Total skeletal muscle mass (SMM) were calculated according to a validated formula by using age and anthropometric measurements. Serum levels of myostatin, tumor necrosis factor (TNF)-α and interleukin-6 were determined by ELISA.
Serum myostatin levels were significantly elevated in COPD patients when compared to controls [(11.85 ± 4.01) ng/ml vs. (7.46 ± 2.21) ng/ml, p < 0.01], while total SMM was significantly decreased in COPD patients when compared to controls [(20.81 ± 1.74) kg vs. (27.31 ± 2.18) kg for male, and (11.70 ± 0.56) kg vs. (19.89 ± 1.47) kg for female] (both p < 0.05). Regression correlation analysis on all COPD patients showed that serum myostatin levels weren't significantly correlated with SMM, but correlated with TNF-α levels (R(2) = 0.042, p = 0.048). However, when stratified for gender, serum myostatin levels were correlated inversely both with SMM (R(2) = 0.20, p = 0.000) and with BMI (R(2) = 0.084, p = 0.019) in subgroup of male patients.
This study demonstrates that circulating myostatin levels are elevated in COPD and related to SMM in male patients, suggesting that myostatin contributes to skeletal muscle wasting in COPD.
肌肉生长抑制素（Myostatin）是骨骼肌质量的负调控因子，与多种肌肉消耗和恶病质相关疾病有关，这一点已得到充分证实。骨骼肌消耗是慢性阻塞性肺疾病（COPD）的一个重要全身表现，而 COPD 患者循环中肌肉生长抑制素的表达尚不清楚。本研究旨在探讨 COPD 患者循环中肌肉生长抑制素的表达及其与骨骼肌消耗的关系。
71 例稳定期 COPD 患者和 60 名年龄匹配的健康对照者参与了这项研究。根据经过验证的公式，使用年龄和人体测量学指标计算总骨骼肌质量（SMM）。通过 ELISA 法测定血清肌肉生长抑制素、肿瘤坏死因子（TNF）-α和白细胞介素（IL）-6水平。
与对照组相比，COPD 患者的血清肌肉生长抑制素水平显著升高[（11.85±4.01）ng/ml 比（7.46±2.21）ng/ml，p<0.01]，而 COPD 患者的总 SMM 明显低于对照组[男性（20.81±1.74）kg 比（27.31±2.18）kg，女性（11.70±0.56）kg 比（19.89±1.47）kg]（均 p<0.05）。对所有 COPD 患者进行回归相关分析显示，血清肌肉生长抑制素水平与 SMM 无显著相关性，但与 TNF-α水平相关（R²=0.042，p=0.048）。然而，按性别分层后，血清肌肉生长抑制素水平与 SMM 呈负相关（R²=0.20，p=0.000），与男性患者的 BMI 呈负相关（R²=0.084，p=0.019）。
本研究表明，COPD 患者循环中肌肉生长抑制素水平升高，与男性患者的 SMM 相关，提示肌肉生长抑制素参与 COPD 患者的骨骼肌消耗。
