Research on tracheal stenosis based on molecular biomarkers

This study, for the first time, identified several key molecular targets associated with tracheal stenosis through integrated clinical, computational, and experimental analyses. Dysregulation of ion channel-related genes (e.g., CACNA1D) and cell cycle regulators (e.g., MKI67, CCNB1, CCNB2) may contribute to stenosis by promoting airway smooth muscle proliferation and calcium signaling disturbances. Conversely, protective markers such as CALML4 and CDKL5 may inhibit proliferation and preserve cellular homeostasis. Notably, respiratory failure may amplify the pro-stenotic effects of MKI67 via enhanced inflammation or oxidative stress. The identified markers (e.g., CACNA1D, MKI67) show promise as early predictors for tracheal stenosis, facilitating early screening and risk stratification. Furthermore, targeted therapies-such as calcium channel blockers-against high-risk markers may offer novel treatment options. However, further studies with larger cohorts and mechanistic experiments are warranted to confirm these findings and explore clinical translation.