Muscle atrophy in chronic obstructive pulmonary disease: molecular basis and potential therapeutic targets.

Abstract

Patients with chronic obstructive pulmonary disease (COPD) experience several systemic manifestations such skeletal muscle dysfunction with and without muscle mass loss. Moreover, frequent comorbidities such as nutritional abnormalities, heart failure, and pulmonary hypertension, which are frequently associated with COPD may further contribute to skeletal muscle mass loss and dysfunction. Muscle dysfunction impairs the patients' exercise capacity and quality of life as daily life activities may be hampered by this problem. Importantly, impaired muscle function and mass loss have been shown to impact negatively on the patients' prognosis and survival in several studies. Thus, this is a major clinical problem that deserves special attention in clinical settings. During the course of exacerbations muscle mass loss takes place, hence aggravating muscle status and performance even after hospital discharge, especially in the frequently exacerbator patients. Several factors and biological mechanisms are involved in the etiology of COPD muscle dysfunction. The biological mechanisms identified so far offer a niche for therapeutic interventions in the patients. In the current review, a general overview of the most relevant etiologic factors and their target biological mechanisms through which muscle mass loss and dysfunction take place in both the respiratory and lower limb muscles in COPD patients is provided. We conclude that more clinical research is still needed targeted to test several therapeutic interventions. Given its prognostic value, the assessment of skeletal muscle dysfunction should be included in the routine evaluation of patients with chronic respiratory disorders and in critical care settings.