DBP, a key characteristic molecule associated with skeletal muscle dysfunction in COPD

Abstract Background Skeletal muscle dysfunction is a prevalent and serious complication of chronic obstructive pulmonary disease (COPD), presenting significant clinical challenges. Despite its commonality, the specific molecules and the mechanisms at play in COPD-related muscle dysfunction remain elusive, leaving a gap in effective early diagnostic and therapeutic strategies. Methods Our study aims to pinpoint the molecular signatures of skeletal muscle dysfunction in COPD by developing both in vivo and in vitro research models, deploying cutting-edge high-throughput sequencing techniques, and employing sophisticated algorithms for dimensionality reduction analysis. Results In our COPD rat models, we observed profound structural changes in the skeletal muscles, such as fiber disruption, mitochondrial shrinkage, and a decrease in mitochondrial count. Notably, we identified DBP—a key molecule—as being markedly overexpressed in COPD models, both in vivo and in vitro. Conclusion Our findings underscore the significant impact COPD has on skeletal muscle structure, leading to muscle wasting, fiber damage, and mitochondrial deterioration. The identification of DBP as a critical molecular marker sheds light on the potential pathways of skeletal muscle impairment in COPD and opens the door for new diagnostic and therapeutic interventions.