International Journal of Chronic Obstructive Pulmonary Disease最新文献

{"title":"Long COVID in Elderly COPD Patients: Clinical Features, Pulmonary Function Decline, and Proteomic Insights.","authors":"Shuangyan Li, Hui Zhao, Min Zhang, Tingting Yuan, Di Chai, Zhengyin Shen, Chengfeng Qin, Yanming Li, Mingming Pan","doi":"10.2147/COPD.S520300","DOIUrl":"10.2147/COPD.S520300","url":null,"abstract":"<p><strong>Background: </strong>Elderly patients with chronic obstructive pulmonary disease (COPD) face a heightened risk of developing long coronavirus disease (COVID); however the exact clinical characteristics and underlying mechanisms remain unclear.</p><p><strong>Methods: </strong>We enrolled 85 elderly COPD patients, of whom 43 reported newly onset persistent fatigue (the most dominant complaint of long COVID) within 1 year after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and they were allocated to the Long-COVID group. The remaining 42 patients were assigned to the Control group. Patients completed questionnaires, pulmonary function tests, chest CT, routine laboratory tests, and blood proteomic analysis.</p><p><strong>Results: </strong>Long-COVID patients had a longer course of COPD (> 5 years, 76.8% vs 52.4%) and duration of SARS-CoV-2 infection (10.0 days vs 7.0 days) (All <i>P</i> < 0.05), higher symptom burden, worse pulmonary ventilation function and a more rapid decrease in DL_CO (All <i>P</i> < 0.05). Proteomic analysis indicated disruptions in inflammation and energy metabolism, potentially underlying long COVID in these patients. The machine learning model identified wheezing, the duration of SARS-CoV-2 infection, EIF2S3 (eukaryotic translation initiation factor 2 subunit gamma), current FEV1/FVC (%), and the course of COPD as key features distinguishing Long-COVID patients, and exhibited excellent performance.</p><p><strong>Conclusion: </strong>Elderly COPD patients with a longer COPD course and duration of COVID-19 are more prone to develop long COVID, with decreased pulmonary ventilation and diffusion ability. Disordered inflammation regulation and energy metabolism may be the potential mechanisms, highlighting the importance of monitoring inflammation and metabolic dysregulation in elderly COPD patients after recovery from COVID-19.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2337-2347"},"PeriodicalIF":2.7,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144627504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictors of Clinical Stability and Mortality in COPD: A Longitudinal Study.","authors":"Wesley Teck Wee Loo, Si Yuan Chew, Jessica Han Ying Tan, Rui Ya Soh, Mariko Siyue Koh, Therese S Lapperre, Pei Yee Tiew","doi":"10.2147/COPD.S531435","DOIUrl":"10.2147/COPD.S531435","url":null,"abstract":"<p><strong>Background: </strong>There is no consensus on the definition of clinical stability in chronic obstructive pulmonary disease (COPD), and it is less frequently used as a treatment target compared to severe asthma. The factors that determine clinical stability and their effects on mortality are less well-studied in patients with COPD.</p><p><strong>Methods: </strong>To address this gap, we conducted a prospective longitudinal cohort study to identify predictors of two-year clinical stability, defined as no exacerbations and stable symptoms (<2 point change in CAT score from baseline), and the impact of comorbid cardiovascular disease (CVD) on clinical stability and mortality in COPD patients.</p><p><strong>Results: </strong>A total of 463 patients (mean age 71 ± 9 years) were enrolled in this study. The cohort was predominantly Chinese (81.7%) and 45.6% of participants were current smokers. The majority (55.7%) had a history of CVD. Approximately 36% of the cohort achieved clinical stability at one year, and one-third achieved stability at two years. Predictors of 2-year clinical stability included higher body mass index (BMI) (p<0.001), higher post-bronchodilator FEV1/FVC ratio (p=0.0132), fewer baseline exacerbations (p=0.007), absence of bronchiectasis (p=0.045), preserved hemoglobin levels (p=0.019), and successful smoking cessation (p=0.039). Notably, while 2-year clinical stability did not predict subsequent mortality, the presence of CVD was a significant predictor of 5-years mortality (HR 1.48, 95% CI 0.99-2.22; p=0.05).</p><p><strong>Conclusion: </strong>Our study identified several predictors of 2-year clinical stability in patients with COPD. However, clinical stability at 2 years did not predict subsequent mortality. These findings suggest that clinical stability and mortality are distinct outcomes that are driven by different sets of predictive variables. This underscores the need for a comprehensive approach to COPD management that not only addresses exacerbations and symptoms, but also considers a broader range of factors influencing survival, particularly the management of comorbidities such as cardiovascular disease.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2311-2324"},"PeriodicalIF":2.7,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12248741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144627420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Marijuana Use and Chronic Obstructive Pulmonary Disease: A Case Report.","authors":"Brenna S Ostertag, Kathryn W Hendrickson","doi":"10.2147/COPD.S520875","DOIUrl":"10.2147/COPD.S520875","url":null,"abstract":"<p><p>Marijuana smoking has become increasingly common in the United States and the world as more states and countries have legalized it for medical and recreational use. There are a number of carcinogens in marijuana smoke similar to those in tobacco smoke, and yet it has been difficult in the literature to find a causal relationship between marijuana smoking and chronic obstructive pulmonary disease (COPD). We present a patient whose main risk factor for emphysema is daily marijuana smoking for upwards of 35 years with no personal history of smoking tobacco, and no other obvious risk factors. Current studies have shown association with chronic marijuana smoking and various lung complaints, forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) ratio, and inconsistently with chronic bronchitis. With this case, we add to the current body of literature that suggests a possible relationship between long-term, heavy marijuana use and COPD.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2305-2309"},"PeriodicalIF":2.7,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144627503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Crucial Role of the PPAR Signaling Pathway in the Diagnosis and Treatment of Chronic Obstructive Pulmonary Disease: An Analysis of Gene Expression and Macrophage Polarization.","authors":"Ling Zhang, Rong Guo, Haixia Wu, Abula Abudusalamu, Wei Ding, Dewei Li, Xuemei Wei, Lin Niu","doi":"10.2147/COPD.S518592","DOIUrl":"10.2147/COPD.S518592","url":null,"abstract":"<p><strong>Purpose: </strong>To explore the role of the peroxisome proliferator-activated receptor (PPAR) signaling pathway in chronic obstructive pulmonary disease (COPD) and identify potential biomarkers and therapeutic targets, given that COPD is a major global health burden and the specific molecular mechanisms of the PPAR pathway in COPD are not fully understood.</p><p><strong>Patients and methods: </strong>Gene expression data from the GEO database were analyzed to identify key genes and immune cells related to COPD. Peripheral blood samples were collected from COPD patients and healthy controls. Key genes were confirmed by PCR, and immune cells were characterized using flow cytometry.</p><p><strong>Results: </strong>Eight core genes associated with the PPAR signaling pathway were identified. NCOA1 and PPARGC1A were downregulated in COPD patients, while NCOR1, NRIP1, and SLC27A5 were upregulated. Receiver operating characteristic (ROC) curve analysis showed that NCOA1, NCOR1, and SLC27A5 have potential for COPD diagnosis. There was a significant increase in the proportion of M2 macrophages in COPD patients, indicating a shift in macrophage polarization towards the M2 phenotype. Genes within the PPAR signaling pathway were closely associated with macrophage polarization state.</p><p><strong>Conclusion: </strong>The research findings provide new biomarkers and potential therapeutic targets for the early diagnosis and personalized treatment of COPD, emphasizing the significant role of the PPAR signaling pathway in the pathogenesis of COPD.</p><p><strong>Clinical trial registry: </strong>The population study involved in this research has been registered under the (chictr.org.cn). Registry identifier: ChiCTR2400086268.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2287-2304"},"PeriodicalIF":2.7,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12248238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144627422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Mechanisms of Lijin Fang on Treg/Th17 Cell Imbalance in COPD Based on Network Pharmacology.","authors":"Zhan-Hua Li, Si-Ning Chen, Ling Pan, Rui Liu, Wei Liang, Mei-Qun Luo, Hai-Fei Liao, Jie Feng, Hao-Zhou Wang, Yue-Gan Huang, Jing-Hui Zheng","doi":"10.2147/COPD.S512469","DOIUrl":"10.2147/COPD.S512469","url":null,"abstract":"<p><strong>Background: </strong>Chronic Obstructive Pulmonary Disease (COPD) is chronic respiratory disease that severely affects patients' quality of life and is associated with high mortality rates. Investigating the imbalance between regulatory T cells (Tregs) and T helper 17 cells (Th17) in COPD treatment is crucial, as this imbalance plays a significant role in the disease's inflammatory processes. This study explores the therapeutic potential of the traditional Chinese medicine(TCM) formula, Lijin Fang (LJF), focusing on its ability to restore Treg/Th17 balance.</p><p><strong>Methods: </strong>We employed bioinformatics and in vitro cell experiments to analyze the active components and targets of LJF. Network pharmacology, differential gene expression, pathway enrichment, ROC model prediction, and immune infiltration analyses were conducted, followed by molecular docking studies. Rat peripheral blood mononuclear cells (PBMCs) were cultured and treated with cigarette smoke extract (CSE) and LJF-containing serum, with flow cytometry, ELISA, and Western blotting used to assess relevant markers.</p><p><strong>Results: </strong>Our findings demonstrate that treatment with (10% or 30%)LJF-containing serum significantly increased the proportion of Treg cells while concurrently decreasing Th17 cell populations in the 5%CSE-treated rat PBMC model (p<0.001). We observed a reduction in pro-inflammatory cytokines such as interleukin-17 (IL-17), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), alongside an increase in the anti-inflammatory cytokine interleukin-10 (IL-10) (p<0.001). Additionally, potential therapeutic targets, including IL-10, potassium voltage-gated channel subfamily N member 4 (KCNN4), and Baculoviral IAP repeat-containing protein 3 (BIRC3), were identified. Molecular docking results indicated stable interactions between IL-10 and BIRC3 with the constituents of LJF.</p><p><strong>Conclusion: </strong>This study highlights LJF's anti-inflammatory potential in restoring the Treg/Th17 balance and regulating cytokine expression in COPD.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2227-2247"},"PeriodicalIF":2.7,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12242538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144610066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prompt versus Delayed Triple Therapy in COPD: Solutions to Time-Related Biases in Observational Studies.","authors":"Samy Suissa, Sophie Dell'Aniello, Michael Andrew Webster-Clark, Pierre Ernst","doi":"10.2147/COPD.S527497","DOIUrl":"10.2147/COPD.S527497","url":null,"abstract":"<p><strong>Background: </strong>Recent observational studies have reported that prompt initiation of single-inhaler triple therapy after a COPD exacerbation is more effective than delayed initiation. We show that their study design, by \"peeking into the future\" to define the timing of treatment initiation, introduces time-related biases, particularly protopathic bias. These biases can be avoided using the \"cloning\" approach to emulate a randomized trial approach.</p><p><strong>Methods: </strong>We formed a cohort of patients with COPD who had an exacerbation (index) after September 2017, using the United Kingdom's Clinical Practice Research Datalink (CPRD). Using the \"cloning\" trial emulation technique, each subject was assigned to both the prompt and the delayed initiator arms as of the index date and censored according to their treatment over time. The Cox model was used to compare the incidence of the first exacerbation after the index exacerbation, over one year, after weighing by inverse probability of censoring. We also replicated the biased approach of the recent studies, based on peeking into the future.</p><p><strong>Results: </strong>The cohort included 91,958 eligible subjects who had an exacerbation, generating 91,958 prompt initiator clones and 91,958 delayed initiator clones. The hazard ratio (HR) of a moderate or severe exacerbation, comparing prompt versus delayed initiators, was 0.98 (95% CI: 0.80-1.19), while it was 1.26 (95% CI: 0.81-1.96) for severe exacerbation. The replication of the time-related biased approach comparing prompt with delayed initiation resulted, correspondingly, in HRs of 0.73 (95% CI: 0.65-0.81) and 0.58 (95% CI: 0.46-0.74).</p><p><strong>Conclusion: </strong>Using a trial emulation approach, prompt treatment with single-inhaler triple therapy after a COPD exacerbation was not more effective than delayed treatment at reducing the incidence of subsequent exacerbations. The method used by previous studies, suggesting significant effectiveness with prompt treatment initiation, was affected by time-related biases induced by peeking into the future. A randomized controlled trial can confirm these findings.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2273-2285"},"PeriodicalIF":2.7,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144601983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Low Hand Grip Strength on Quality of Life, Utilization of Healthcare, and Mental Health in Individuals with Airflow Limitation.","authors":"Sang Hyuk Kim, Sungmin Zo, Sung A Kong, Ju Hee Cho, Jong Geol Do, Sun Hye Shin, Hye Yun Park","doi":"10.2147/COPD.S510974","DOIUrl":"10.2147/COPD.S510974","url":null,"abstract":"<p><strong>Purpose: </strong>A higher prevalence of sarcopenia has been demonstrated in individuals with airflow limitation (AFL). However, data on the impact of sarcopenia on quality of life, utilization of healthcare, and mental health in individuals with AFL are limited.</p><p><strong>Patients and methods: </strong>We used data from the 2014-2019 Korea National Health and Nutrition Examination Survey (KNHANES), and participants with AFL were included. Sarcopenia was assessed using hand grip strength (HGS). The outcomes were health-related quality of life (HRQoL), utilization of healthcare, and mental health. The impact of low HGS and outcomes was assessed using multivariable logistic regression analysis.</p><p><strong>Results: </strong>Among participants with AFL, 12.6% had low HGS and the median (interquartile range) of HGS was 22.5 (18.9-26.1) kg for women and 37.7 (32.9-42.6) kg for men. After adjusting for confounders, low HGS was associated with a decrease in HRQoL (usual activities: adjusted odds ratio [aOR], 1.70; 95% confidence interval [CI], 1.14-2.54; pain/discomfort: aOR, 1.44; 95% CI, 1.02-2.02, anxiety/depression: aOR, 1.59; 95% CI, 1.05-2.41), and increased perceived stress (aOR, 1.77; 95% CI, 1.24-2.53). In the subgroup analysis, the impact of low HGS on HRQoL, utilization of healthcare, and mental health was more evident in the reduced lung function and inactive physical activity groups.</p><p><strong>Conclusion: </strong>Overall, low HGS was associated with decreased quality of life and worsening mental health in participants with AFL. Our findings underscore the importance of muscle strength for HRQoL, particularly in those with impaired lung function and sedentary lifestyles, suggesting that regular physical activity including muscle-strengthening exercises may improve HRQoL.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2199-2210"},"PeriodicalIF":2.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144601982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential Causal Relationship Between Chronic Obstructive Pulmonary Disease and Diabetes: A Bidirectional Two-Sample Mendelian Randomization Study.","authors":"Xinyan Wang, Xin Chen, Ruizhi Feng, Hongli Jiang, Wei Liu","doi":"10.2147/COPD.S516346","DOIUrl":"10.2147/COPD.S516346","url":null,"abstract":"<p><strong>Purpose: </strong>Diabetes, particularly type 2 diabetes (T2D), is a common comorbidity that occurs at a higher frequency in chronic obstructive pulmonary disease (COPD) patients compared to the general population. The COPD-diabetes association is documented epidemiologically and experimentally. Potential mechanisms, including systemic inflammation and metabolic dysregulation, are discussed as plausible pathways. However, their causal relationship still needs to be confirmed.</p><p><strong>Methods: </strong>We conducted a comprehensive bidirectional two-sample Mendelian randomization (MR) analysis to evaluate the causal links between COPD and both type 1 diabetes (T1D) and T2D by using genome-wide association study (GWAS) summary statistics in European and Asian populations. By employing MR methods, the causal effect of diabetes on the risk of COPD as well as specific COPD-related clinical outcomes, including COPD with infections (COPD-I), pneumonia or pneumonia-derived septicaemia, chronic opportunistic infections, respiratory insufficiency, hospital admissions, and onset age (early or late) were explored.</p><p><strong>Results: </strong>Forward MR analysis provided evidence consistent with a causal relationship between T2D and an increased risk of COPD in the European population (IVW odds ratio (OR): 1.002, 95% confidence interval (CI): 1.001-1.003, <i>P</i> = 0.001). This association appeared consistent with MR Egger analysis, yielding a similar result for European COPD patients (MR Egger OR: 1.108, 95% CI: 1.016 -1.208, <i>P</i> = 0.021). No statistically conclusive evidence of a causal relationship between diabetes and COPD was found in the Asian population. Besides, genetically determined T1D was identified as a risk factor for the incidence of COPD-I in the European-specific population (IVW OR: 1.017, 95% CI: 1.009-1.025, <i>P</i> < 0.001). The reverse MR analysis, exploring the effect of COPD on the risk of diabetes, did not achieve consistent results in either the European or Asian populations.</p><p><strong>Conclusion: </strong>This study suggested a modest but statistically significant causal association between T2D and COPD in individuals of European ancestry. Further explorations are required to better understand the underlying mechanisms linking diabetes to COPD development.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2259-2272"},"PeriodicalIF":2.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144592757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adolescent and Current Exercise Habits in Chronic Obstructive Pulmonary Disease: Associations with Body Composition, Physical Activity, and Pulmonary Function.","authors":"Tomoko Iriyama, Yumiko Matsuo, Yoko Tsunoda, Akio Yamazaki, Yasuki Uchida, Hiroaki Nakagawa, Daisuke Kinose, Masafumi Yamaguchi, Yasutaka Nakano, Emiko Ogawa","doi":"10.2147/COPD.S517494","DOIUrl":"10.2147/COPD.S517494","url":null,"abstract":"<p><strong>Purpose: </strong>Regular exercise significantly influences chronic obstructive pulmonary disease (COPD) outcomes. However, the associations of exercise habits during adolescence compared to current exercise habits on physical activity (PA), body composition, pulmonary function, and CT imaging parameters remain unclear. Therefore, the present study aimed to clarify the associations of adolescent and current exercise habits with current conditions.</p><p><strong>Patients and methods: </strong>This cross-sectional study enrolled 86 participants, including 72 with COPD and 14 with pre-COPD. Adolescent exercise habits were defined as regular exercise during ages 16 to 22 years, while current exercise habits were defined as regular exercise for at least 1 year. PA was assessed using a triaxial accelerometer, body composition was assessed using bioelectrical impedance analysis, and pulmonary function was assessed using spirometry and computed tomography.</p><p><strong>Results: </strong>Adolescent exercise habits were not significantly associated with PA or body composition, although they were associated with an increased lung volume. Compared to adolescent exercise habits, current exercise habits were associated with an increased duration of active engagement, less sedentary behavior, and increased diffusing capacity. Moreover, current exercise habits were associated with increased fat-free mass index, bone mineral content, and phase angle, which is an indicator of muscle quality. The influence of current exercise habits on these musculoskeletal indicators remained significant even after adjusting for age, sex, disease severity, and adolescent exercise habits. In addition, the relationship between PA and musculoskeletal health was more pronounced in patients with moderate-to-severe COPD than in those with mild COPD.</p><p><strong>Conclusion: </strong>Exercise during adolescence may promote increased lung volume. However, even after the onset of COPD, especially if the disease has progressed, regular exercise routines can help maintain PA, better body composition, and pulmonary function.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2249-2257"},"PeriodicalIF":2.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144601980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effective-Component Compatibility of Bufei Yishen Formula III Protects Lung Air-Blood Barrier by Regulating the Oxidative Stress: via the Nuclear Factor-E₂-Related Factor 2 Pathway.","authors":"Kexin Xu, Xuejie Shao, Ruilong Lu, Yixi Liao, Yakun Zhao, Bo Wang, Zhiguang Qiu, Yange Tian","doi":"10.2147/COPD.S513071","DOIUrl":"10.2147/COPD.S513071","url":null,"abstract":"<p><strong>Purpose: </strong>Bufei Yishen formula (BYF) is an effective treatment strategy for chronic obstructive pulmonary disease (COPD). Effective-component compatibility of BYF III (ECC-BYF III), composed of 5 active ingredients (ginsenoside Rh1, paeonol, astragaloside, icariin and nobiletin) from BYF, has similar effects to BYF in intervening COPD. The abnormal structure and hypofunction of lung air-blood barrier induces inefficiency gas exchange and promotes development of COPD. However, the role of ECC-BYF III in the air-blood barrier remains unknown. This study dedicated to exploring the effect and mechanism of ECC-BYF III improve structure and function of lung air-blood barrier in COPD.</p><p><strong>Methods: </strong>A COPD rat model was established to study the treatment of ECC-BYF III against COPD. The protective effect of ECC-BYF III on COPD was evaluated through pulmonary function and lung tissue pathology. The structure damage of the lung air-blood barrier was assessed using electron microscopy and immunofluorescence. Finally, we proved the regulating effect of ECC-BYF III in oxidative via the Nrf2 pathway.</p><p><strong>Results: </strong>The ECC-BYF III could significantly alleviate reduced pulmonary function, decrease damage of lung tissue and regulate oxidative stress in COPD rats. And ECC-BYF III reduced thickness of respiratory membrane, ameliorated damage of pulmonary capillary endothelial cells (PCECs) and alveolar epithelial cells (AECs) in COPD rats. Also, ECC-BYF III protected the function and normal cell morphology of type I alveolar epithelial cell (AT I) and type II alveolar epithelial cell (AT II) in COPD rats. Lastly, ECC-BYF III was indicated to adjust the Nrf2 pathway to improve oxidative stress and protect lung air-blood barrier in COPD rats.</p><p><strong>Conclusion: </strong>ECC-BYF III protects lung air-blood barrier in COPD by regulating oxidative stress via Nrf2 pathway.</p>","PeriodicalId":48818,"journal":{"name":"International Journal of Chronic Obstructive Pulmonary Disease","volume":"20 ","pages":"2211-2226"},"PeriodicalIF":2.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144601981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}