Time‐resolved proteomic profiling of cigarette smoke‐induced experimental chronic obstructive pulmonary disease

Background and objective Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness death worldwide. Current treatments aim to control symptoms with none able reverse or stop its progression. We explored major molecular changes in COPD pathogenesis. Methods employed quantitative label-based proteomics map lung tissue proteome cigarette smoke-induced experimental that induced over 8 weeks progresses 12 weeks. Results Quantification 7324 proteins enabled tracking proteome. Alterations protein expression profiles occurred induction phase, 18 16 at 4- 6-week time points, compared age-matched controls, respectively. Strikingly, 269 had altered after when hallmark pathological features human emerge, but this dropped 27 Differentially expressed were validated using other mouse bronchial biopsy samples. Major RNA biosynthesis (heterogeneous nuclear ribonucleoproteins C1/C2 [HNRNPC] RNA-binding Musashi homologue 2 [MSI2]) modulators inflammatory responses (S100A1) notable. Mitochondrial dysfunction oxidative stress also occurred. Conclusion provide a detailed proteomic profile, identifying associated pathogenesis progression establishing platform develop effective new treatment strategies.