Autophagy is a process of cell self-renewal that is dependent on the degradation of the cytoplasmic proteins or organelles of lysosomes. Many diseases, such as metabolic diseases, cancer, neurodegenerative diseases, and lung diseases, have been confirmed to be associated with elevated or impaired levels of autophagy. At present, studies have found that autophagy participates in the regulation of chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis, pulmonary hypertension, acute lung injury, lung cancer, and other pulmonary diseases. Using recent literature on the signal transduction mechanisms of autophagy and the effects of autophagy signalling on lung diseases, this review intends to clarify the mechanisms of lung disease to guide the treatment of related diseases. The reviews of this paper are available via the supplemental material section.

This study aimed to validate the chronic obstructive pulmonary disease (COPD) Population Screener (COPD-PS) questionnaire as a screening tool in a cohort of Chinese subjects who underwent a health examination, and to summarise its overall performance through a meta-analysis. We enrolled 997 subjects aged ≥40 years who underwent a health examination, both lung function and COPD-PS data were collected. The screening performance of COPD-PS was evaluated with a receiver operating characteristic (ROC) curve analysis, using the area under the curve (AUC) to assess the screening accuracy. A standard diagnostic meta-analysis was used to summarise the screening performance of COPD-PS for COPD. Of the 997 subjects, 157 were identified as having COPD. The COPD-PS score was significantly higher in COPD patients than controls (5.03 ± 5.11 vs. 2.72 ± 1.80, p < .001). At a cut-off of 4, the sensitivity and specificity of COPD-PS for identifying COPD were 74.52 and 70.24%, respectively, with an AUC of 0.79. Eight studies (including this study) were included in this meta-analysis. The pooled estimates for COPD-PS were as follows: sensitivity of 0.66 (95% CI: 0.47–0.63), specificity of 0.86 (95% CI: 0.84–0.89), positive likelihood ratio of 3.00 (95% CI: 1.65–5.47), negative likelihood ratio of 0.43 (95% CI: 0.35–0.52) and diagnostic odds ratio of 7.24 (95% CI: 3.91–13.40). The AUC of the summary ROC curve was 0.78. COPD-PS appears to be a useful tool for screening individuals with a high risk of COPD and guiding the selection of individuals for subsequent spirometry examination.

The airway and lung tissue inflammation and structural changes caused by COPD lead to persistent and irreversible airflow limitation in patients. Several studies have associated IL-17A with COPD airway inflammation and collagen deposition, while autophagy is essential for maintaining normal cell function. Based on these findings, we propose a hypothesis that IL-17 affecting the autophagy of macrophages through the PI3K/AKT/mTOR pathway may contribute to the regulation of the airway remodeling process in COPD. The COPD airway remodelling model was confirmed by pulmonary function tests and HE and Masson staining. IL-17A, IL-6 and CCL20 were detected by ELISA, autophagosomes (APs) were observed by transmission electron microscopy, and western blotting was used to detect PI3K/AKT/mTOR-related proteins, autophagy-related proteins and collagen. Immunofluorescence revealed colocalization of LC3 in mouse bronchial fibroblasts (MBFs). MBFs were isolated and cultured via lentiviral transfection, IL-17RA overexpression or silencing, and quantitative analysis of PI3K/AKT/mTOR pathway-related proteins and autophagy-related proteins via western blotting. The results validated the establishment of the COPD model. Increased IL-17A in the COPD airway and increased IL-6 and CCL20 expression were observed in the COPD mice supplemented with the autophagy inhibitor 3MA. Using TEM, we observed a significant reduction in the number of APs in the airways in both the COPD and 3MA groups. Moreover, the PI3K/AKT/mTOR pathway phospho-p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR ratios were also increased in the COPD group. Moreover, as P62 increased, Beclin-1 and LC3II/I expression decreased correspondingly, while Collagen I and Collagen III also increased. In our study of cultured mouse MBFs, the results showed that overexpression (OE) virus-mediated transfection of MBFs overexpressing IL-17RA increased the p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR ratios, increased the P62 content and reduced the expression of Beclin-1 and LC3II/I. However, compared with the OE group, the silencing (sh)-mediated transfection of MBFs with IL-17RA had almost opposite effects. Increased collagen production and the expression of IL-17A, IL-6 and CCL20 in the airways of COPD mice. Autophagy decreased, and the PI3K/AKT/mTOR pathway was activated in COPD airway tissue. In primary cultured MBFs from COPD mice, IL-17A combined with IL-17RA activates the PI3K/AKT/mTOR pathway, thereby inhibiting autophagy.

Background: Chronic obstructive pulmonary disease (COPD) is a significant global health issue, suspected to elevate the risk for various cancers. This study sought to discern whether COPD serves as a risk marker or a causative factor for prevalent cancers. Methods: We employed univariable MR (UVMR) analyses to investigate the causal relationship between COPD and the top ten common cancers. Sensitivity analyses were performed to validate the main findings. Multivariable MR (MVMR) and two-step MR analyses were also conducted. False-discovery-rate (FDR) was used to correct multiple testing bias. Results: The UVMR analysis demonstrated notable associations between COPD and lung cancer (odds ratio [OR] = 1.42, 95%CI 1.15–1.77, FDR = 6.37 × 10^–3). This relationship extends to lung cancer subtypes such as squamous cell carcinoma (LUSC), adenocarcinoma (LUAD), and small cell lung cancer (SCLC). A tentative link was also identified between COPD and bladder cancer (OR = 1.53, 95%CI 1.03–2.28, FDR = 0.125). No significant associations were found between COPD and other types of cancer. The MVMR analysis that adjusted for smoking, alcohol drinking, and body mass index did not identify any significant causal relationships between COPD and either lung or bladder cancer. However, the two-step MR analysis indicates that COPD mediated 19.2% (95% CI 12.7–26.1%), 36.1% (24.9–33.2%), 35.9% (25.7–34.9%), and 35.5% (26.2–34.8%) of the association between smoking and overall lung cancer, as well as LUAD, LUSC, and SCLC, respectively. Conclusions: COPD appears to act more as a risk marker than a direct cause of prevalent cancers. Importantly, it partially mediates the connection between smoking and lung cancer, underscoring its role in lung cancer prevention strategies.

Background: In this study, we established a chronic obstructive pulmonary disease (COPD) model by stimulating mice with cigarette smoke, and observed the effects of dendritic cells (DCs) overexpressing SOCS1 on Th17, Treg and other related cytokines in peripheral blood, bronchoalveolar lavage fluid and lung tissues of COPD mice.Methods: After successfully transfecting DCs with overexpressing SOCS1 (DC-SOCS1), the mice were injected with DC-SOCS1 (1 × 10⁶), DC-SOCS1 (2 × 10⁶) and immature DCs (1 × 10⁶) via tail vein on days 1 and 7 of COPD fumigation modeling. After day 28 of modeling, the peripheral blood, BALF and lung tissue samples were extracted from the mice, and the changes of DCs, Th17 and Treg cells and related cytokines were detected by immunohistochemistry, immunofluorescence, HE staining, flow cytometry and ELISA.Results: The results showed that DC-SOCS1 was able to reduce the secretion of pro-inflammatory factors and increase the anti-inflammatory factors in the COPD mice, and the effect of high concentration (2 × 10⁶DC-SOCS1) was better than low concentration (1 × 10⁶DC-SOCS1). Moreover, the intervention effect was significant on day 1 compared with day 7. In the mice injected with DC-SOCS1, the expression of CD83, IL-4, Foxp3, and CCR6 was increased on day 1 than those on day 7, while IL-17 and IFN-γ was decreased.Conclusions: Intervention of COPD mice with high concentrations of DCs-SOCS1 reduced pro-inflammatory factor secretion and attenuated the inflammatory response in COPD.Trial registrationNot applicable.

A 66-year-old woman had two severe episodes of massive hemoptysis without any premonitory symptoms, with approximately 400–500 ml blood each time. Bronchoscopic exam revealed a smooth and pulsatile protrusion that was approximately 8–10 mm in diameter found at the beginning of the right middle lobe bronchus in the bronchial lumen. The protrusion arose from the surface with absolutely normal mucosa. Selective bronchial arteriography showed that elongated, tortuous, and dilated branches of the bronchial artery in the region of the middle lobe bronchus. Further bronchial arterial embolization (BAE) is recommended, although the patient currently has no active bleeding. Bronchial Dieulafoy’s disease (BDD) is a rare and life-threatening disease. Selective bronchial arteriography is a diagnostic tool to detect and locate abnormal arteries. There is no unified guideline or expert consensus on the treatment of BDD. Selective BAE or surgical resection is usually used as a first-line treatment to control hemoptysis. The reviews of this paper are available via the supplemental material section.