Osteoporosis, Sarcopenia and Muscle-bone Crosstalk in COPD

Chronic obstructive pulmonary disease (COPD) is a prevalent chronic airway disease characterized by persistent airflow limitation and daily respiratory symptoms. The pathological hallmark of the disease is alveolar destruction and airway inflammation, usually associated with significant exposure to noxious particles or gases, most importantly cigarette smoking. COPD is now viewed as a systemic disease with significant comorbidities, such as skeletal muscle loss/sarcopenia, osteoporosis, cardiovascular diseases, lung cancer, sleep apnea, metabolic syndrome, anxiety and depression, which contribute markedly to the morbidity and mortality of COPD.

Skeletal muscle dysfunction/sarcopenia and osteoporosis are common in COPD, and their pathogenic mechanisms are generally believed to be associated with systemic inflammation. However, muscle and bone are closely linked spatially, and in addition to mechanical interactions, they also serve as endocrine organs by producing myokines and osteokines to regulate bone metabolism and muscle growth and functions reciprocally, a mechanism called muscle-bone crosstalk. In recent years, advances have been made in understanding the link between COPD and its musculoskeletal comorbidites. However, detailed molecular mechanisms underlying osteoporosis, sarcopenia and muscle-bone crosstalk in COPD remain to be fully explored, targeting of which could facilitate development of novel therapeutics. In addition, new technologies and platforms enabling better assessments of musculoskeletal pathophysiology in COPD are needed.

This research topic will cover but not limited to the following areas:
- Myokines and osteokines in human and animal models of COPD.
-Systemic inflammation and musculoskeletal comorbidies of COPD.
-New modalities for assessing skeletal muscle and bone pathophysiology in COPD.
-Exercise/rehabilitation and musculoskeletal pathophysiology in COPD.