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].