Advancing Biomarker‑Driven Therapeutic Strategies in COPD by Linking CC16 Biology to Disease Modification
- Understand how loss of airway epithelial integrity, reflected by reduced CC16 levels, defines biologically distinct COPD endotypes and enables patient stratification beyond symptoms and exacerbation history toward underlying disease mechanisms
- Gain insight into how CC16, when integrated with complementary biomarkers such as sRAGE and fibrinogen, informs prediction of lung function decline, emphysema progression, and therapeutic responsiveness using human translational and longitudinal datasets
- Highlighting how replacement and augmentation of SCGB1A1 directly targets epithelial dysfunction, inflammation, and fibrosis, supporting a disease‑modifying treatment strategy that goes beyond bronchodilation to preserve lung function and reduce exacerbation burden