Background Continual contact with tobacco smoke or biomass fuels induces oxidative apoptosis and stress in bronchial epithelium, which is among the most significant pathogenic mechanisms of chronic obstructive pulmonary disease (COPD). determine the predicted binding site of miR-194-3p and potential targets. Results In our study, we found that PM2.5 significantly aggravated apoptosis in cigarette-inflamed HBEpiCs.… Continue reading Background Continual contact with tobacco smoke or biomass fuels induces oxidative