The loss of alveolar structure and airspace enlargement are major pathological changes in chronic obstructive pulmonary disease (COPD). Type II alveolar epithelial cells (AECII) are involved in maintaining lung tissue repair and alveolar homeostasis. Long non‑coding RNAs (lncRNAs) are involved in multi‑regulating gene transcription, affecting processes including embryonic development, cell differentiation and cellular senescence. The primary aim of the present study was to explore the mechanisms of AECII senescence regulated by lncRNA‑mediated sirtuin 1 (SIRT1) and forkhead box O 3a (FoxO3a) signaling pathways in patients with COPD. Lung tissues from patients with COPD exhibited pathological characteristics and significantly increased senescence‑associated β‑galactosidase activity. Furthermore, the expression levels of senescence‑associated lncRNA1 (SAL‑RNA1), SIRT1 and FoxO3a were reduced, but SAL‑RNA2, SAL‑RNA3, p53 and p21 were upregulated in the lung tissues of patients with COPD compared with control. The results of the present study indicated that lncRNA‑mediated SIRT1/p53 and FoxO3a signaling pathways may regulate AECII senescence in the pathogenesis of COPD, which may provide a novel experimental basis for the treatment of COPD.

In chronic obstructive pulmonary disease (COPD), two major pathological changes that occur are the loss of alveolar structure and airspace enlargement. To treat COPD, it is crucial to repair damaged lung tissue and regenerate the lost alveoli. Type II alveolar epithelial cells (AECII) play a vital role in maintaining lung tissue repair, and amniotic fluid-derived mesenchymal stromal cells (AFMSCs) possess the characteristics of regular mesenchymal stromal cells. However, it remains untested whether transplantation of rat AFMSCs (rAFMSCs) might alleviate lung injury caused by emphysema by increasing the expression of surfactant protein (SP)A and SPC and inhibiting AECII apoptosis. We analyzed the phenotypic characteristics, differentiation potential, and karyotype of rAFMSCs, which were isolated from pregnant Sprague–Dawley rats. Moreover, we examined the lung morphology and the expression levels of SPA and SPC in rats with emphysema after cigarette-smoke exposure and intratracheal lipopolysaccharide instillation and rAFMSC transplantation. The ability of rAFMSCs to differentiate was measured, and the apoptosis of AECII was evaluated. In rAFMSCs, the surface antigens CD29, CD44, CD73, CD90, CD105, and CD166 were expressed, but CD14, CD19, CD34, and CD45 were not detected; rAFMSCs also strongly expressed the mRNA of octamer-binding transcription factor 4, and the cells could be induced to differentiate into adipocytes and osteocytes. Furthermore, rAFMSC treatment up-regulated the levels of SPA, SPC, and thyroid transcription factor 1 and inhibited AECII apoptosis, and rAFMSCs appeared to be capable of differentiating into AECII-like cells. Lung injury caused by emphysema was alleviated after rAFMSC treatment. rAFMSCs might differentiate into AECII-like cells or induce local regeneration of the lung alveolar epithelium in vivo after transplantation and thus could be used in COPD treatment and lung regenerative therapy.

Bronchopleural fistula is a potentially fatal disease most often caused after pneumonectomy. Concomitant problems such as pulmonary infection and respiratory failure are typically the main contributors to patient mortality because of the improper contact between the bronchial and pleural cavity. Therefore, bronchopleural fistulas need immediate treatment, which requires the accurate location and timely closure of the fistula. Currently, bronchoscopic interventions, because of their flexibility and versatility, are reliable alternative therapies in patients for whom surgical intervention is unsuitable. Possible interventions include bronchoscopic placement of blocking agents, atrial septal defect (ASD)/ventricular septal defect (VSD) occluders, airway stents, endobronchial valves (EBVs) and endobronchial Watanabe spigots (EWSs). Recent developments in mesenchymal stem cells (MSCs) transplantation technology and three-dimensional (3D) printed stents have also contributed to the treatment of bronchopleural fistula, but more research is needed to investigate the long-term benefits. This review focuses on the effectiveness of various bronchoscopic measures for the treatment of bronchopleural fistula and the directions for future development.

Heme oxygenase 1 (HMOX1) plays an important role in the development of chronic obstructive pulmonary disease (COPD). However, the association of HMOX1 length polymorphism in promoter region to the risk and severity of COPD has not been well studied. In this study, we searched the databases including PubMed, EMBASE, Cochrane Library and China National Knowledge Infrastructure (CNKI) and extracted the information from related articles. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to study the effect of HMOX1 polymorphism on the risk and severity of COPD. As a result, nine studies were included for this meta‐analysis. Higher frequencies of L allele and type I genotype (containing at least one L allele) were found in patients with COPD (for L allele, OR 2.02, 95% CI: 1.32–3.11, P = 0.001; for type I genotype, OR 1.82, 95% CI: 1.28–2.61, P = 0.001), especially in Asian population (for L allele, OR 2.23, 95% CI: 1.68–2.95, P < 0.001; for type I genotype, OR 2.02, 95% CI: 1.51–2.70, P < 0.001). Genotyping method, source of control subjects, literature quality and language also affected the results to some extent. However, there was little difference in HMOX1 genotypes distribution in patients with COPD with different severity. Our study indicated L allele and type I genotype were related to the susceptibility but not the severity of COPD.

Secondary resistance is a major limitation in the efficacy of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor treatment of lung cancer. Previous studies have shown that expression of the long non‑coding RNA HOX transcript antisense RNA (HOTAIR) is upregulated in lung cancer, which is correlated with metastasis and poor prognosis. However, the precise role of HOTAIR and its effects on gefitinib resistance in human lung adenocarcinoma are not known. To address this issue, in the present study we established a gefitinib‑resistant (R)PC‑9 human lung adenocarcinoma cell line and examined cell viability with the 3‑(4,5‑dimethylthiazol‑2‑yl)‑5‑(3‑carboxymethoxyphenyl)‑2‑ (4‑sulfophenyl)‑2H‑tetrazolium assay. We found that gefitinib concentrations <10 µM inhibited the viability of PC‑9 but not RPC‑9 cells in a dose‑dependent manner. Lentivirus‑mediated HOTAIR RNA interference induced cell apoptosis and S‑phase arrest, as determined by terminal deoxynucleotidyl transferase‑mediated dUTP nick end labeling and flow cytometry. Consistent with these observations, HOTAIR suppression was associated with tumor shrinkage and restoration of gefitinib sensitivity in RPC‑9 xenograft mice. Immunohistochemical analyses and western blot revealed that HOTAIR silencing resulted in the upregulation of B cell lymphoma 2‑associated X protein (Bax), Caspase‑3 and transforming growth factor α (TGF‑α) and downregulation of EGFR and B cell lymphoma 2 (Bcl‑2) levels. These results indicate that HOTAIR normally prevents the activation of Bax/Caspase‑3 while inducing TGF‑α/EGFR signaling. Thus, targeting HOTAIR may be a novel therapeutic strategy for treating gefitinib‑resistant lung adenocarcinoma.