2.2COPD
Airflow limitation with persistent respiratory symptoms and lung chronic inflammation are the main features of COPD, which is characterized by typical, prolonged dyspnea, cough and sputum, mainly due to long-term immune response brought on smoking, occupational exposure, etc.[44]. Increasing studies have shown that lncRNAs and miRNAs may be closely related to the occurrence and development of COPD, could be potential biomarkers and therapeutics[45]. As a predictor of susceptibility, NEAT1 is also associated with disease severity and inflammation level, has increased expression in the peripheral blood of COPD patients, and functions in this way by down-regulation the expression of miR-193a[46]. As a therapeutic way, RNA drugs are highly specific and safe, may be one of the ideal method of administration for COPD[44]. miR-146 affects pulmonary bronchial epithelial cells to have anti-inflammatory effects in a number of chronic lung disorders. Since lnc-PVT1 affects miR-146, its expression level can be utilized to distinguish acute exacerbation of COPD (AECOPD) patients and stable cope patients. lnc-PVT1 expression also predicting COPD susceptibility and AECOPD risk, and is positively correlated with inflammation factors and disease severity stages[47].Through RNA sequencing and Bioinformatics prediction, Qian et al. Created a miRNA-mRN-lncRNA ternary interaction network in non-smoking COPD patients and projected that miR-218-5p/miR15a-RORA-LOC101928100/LINC00861 and miR-218-5p/miR15a-TGF3-RORA-AS1 interactions play a significant role in the pathogenesis of non-smoking COPD patients[48].
Inducing oxidative stress from cigarette smoking results in severe cellular damage and an inflammatory response, which is a key pathogenic aspect of COPD. When cigarette smoke is applied to cells in vitro, it can cause cytotoxicity and an immunological response. Bronchial epithelial cells treated with smoke extraction have higher levels of lncRNA MEG3, which causes higher cell apoptosis and inflammation by sponge binding to miR-181a-2-3p [49]. Since lnc RP11-86H7.1 interacted with miR-9-5p through a ceRNA mechanism, which would lower miR-9-suppression 5p’s of NFKB1 production in bronchial epithelial cells, Zhao et al. hypothesized that such ternary network may boost PM2.5 related COPD[50].