Abstract

OBJECTIVE:Muscle wasting contributes to the reduced quality of life and increased mortality in chronic obstructive pulmonary disease (COPD). Muscle atrophy in mice with cachexia was caused by Activin A binding to ActRIIB. The role of circulating Activin A leading to muscle atrophy in COPD remains elusive.METHODS:In the present study, we evaluated the relationship between serum levels of Activin A and skeletal muscle wasting in COPD patients. The expression levels of serum Activin A were measured in 78 stable COPD patients and in 60 healthy controls via ELISA, which was also used to determine the expression of circulating TNF-α levels. Total skeletal muscle mass (SMM) was calculated according to a validated formula by age and anthropometric measurements. The fat-free mass index (FFMI) was determined as the fat-free mass (FFM) corrected for body surface area.RESULTS:Compared to the healthy controls, COPD patients had upregulated Activin A expression. The elevated levels of Activin A were correlated with TNF-α expression, while total SMM and FFMI were significantly decreased in COPD patients. Furthermore, serum Activin A expression in COPD patients was negatively associated with both FFMI and BMI.CONCLUSION:The above results showed an association between increased circulating Activin A in COPD patients and the presence of muscle atrophy. Given our previous knowledge, we speculate that Activin A contributes to skeletal muscle wasting in COPD.

Highlights

  • As a degenerative systemic manifestation, skeletal muscle atrophy contributes to a determinant of mortality independent of airway obstruction in chronic obstructive pulmonary disease (COPD) [1,2]

  • The current study reveals that elevated circulating levels of Activin A (Act A) in COPD are associated with muscle atrophy as shown by reductions in body mass index (BMI), skeletal muscle mass (SMM) and fat-free mass index (FFMI)

  • Several previous studies explored that muscle atrophy as a systemic complication of whole body weight is commonly detected in 10%-40% of COPD patients [19]

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Summary

Introduction

As a degenerative systemic manifestation, skeletal muscle atrophy contributes to a determinant of mortality independent of airway obstruction in chronic obstructive pulmonary disease (COPD) [1,2]. Skeletal muscle atrophy as selective depletion of fat-free mass index (FFMI) and body mass index (BMI) disturbs the potential balance of muscle protein synthesis and degradation in 20-40% of COPD patients depending on definition and disease stage, resulting in decreased muscle function and adaptive capacity [3,4]. Total skeletal muscle mass (SMM) constitutes more than half of the total body mass. As an important indicator of nutrition and metabolic function, declining SMM is recognized as having adverse effects on health [5,6]. No potential conflict of interest was reported

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