miR-766-5p Attenuates Cigarette Smoke-Induced COPD by Targeting MAPK1

Chronic obstructive pulmonary disease (COPD) represents a significant health burden in older individuals, and early diagnosis remains a challenge. miR-766-5p is dysregulated in COPD. However, its specific role and underlying mechanisms remain unclear. Exploring the diagnostic value of miR-766-5p in COPD and its protective mechanism through targeting MAPK1 holds significant clinical importance for the identification of novel biomarkers and therapeutic targets. Serum samples were obtained from elderly COPD patients and healthy controls to measure miR-766-5p expression and analyze its clinical significance. In vitro, a cigarette smoke extract (CSE)-induced injury model was established using BEAS-2B cells. Transfection was employed to alter the expression of miR-766-5p and MAPK1, followed by assessments of cell viability, inflammatory responses, oxidative stress, and epithelial-mesenchymal transition (EMT). The direct targeting relationship was confirmed by a dual-luciferase reporter assay. Serum miR-766-5p expression was significantly downregulated in COPD patients compared to healthy controls. Its level showed a positive correlation with pulmonary function and demonstrated diagnostic value for COPD. In cellular experiments, overexpression of miR-766-5p alleviated CSE-induced reductions in cell viability, the release of inflammatory factors (IL-6, IL-1β, TGF-β1), oxidative stress (increased MDA and decreased SOD), and EMT. Mechanistically, MAPK1 was identified as a direct target of miR-766-5p. Furthermore, overexpression of MAPK1 reversed the protective effects of miR-766-5p against CSE-induced cellular injury. miR-766-5p is markedly reduced in COPD and holds potential as a diagnostic biomarker. It exerts a protective role against airway epithelial cell injury by targeting and inhibiting MAPK1.