Chinese medical journal pulmonary and critical care medicine最新文献

{"title":"Artificial intelligence in respiratory medicine: From diagnosis to treatment and future directions","authors":"Zhe Chen,&nbsp;Zhiyong Tang,&nbsp;Rob M. Ewing,&nbsp;Zehor Belkhatir,&nbsp;Yihua Wang","doi":"10.1016/j.pccm.2026.05.005","DOIUrl":"10.1016/j.pccm.2026.05.005","url":null,"abstract":"<div><div>Lung diseases—including lung cancer, chronic obstructive pulmonary disease (COPD), asthma, interstitial lung diseases (ILDs), and rare conditions like cystic fibrosis—remain major drivers of global morbidity and mortality. Timely diagnosis and individualized treatment are frequently challenged by heterogeneous clinical phenotypes and the complexity of multimodal data. This review provides a critical synthesis of the transformative role of artificial intelligence (AI) in respiratory care, tracing the paradigm shift from classical machine learning to emerging large language models (LLMs) and multimodal foundation models. We evaluate the performance of AI across the patient care continuum: beginning with radiologist-level nodule detection and automated diagnostics, advancing into AI-powered clinical decision support systems (CDSS) and surgical/radiotherapeutic interventions, and culminating in prognostic modeling and “digital twin” simulations for longitudinal patient management. Furthermore, we explore the translational frontier of precision medicine, examining how AI leverages multi-omics and liquid biopsies to drive novel biomarker discovery and accelerate drug repurposing. Finally, we address persistent sociotechnical barriers—including data sovereignty, legal liability, and the critical need for prospective clinical validation—proposing a translational roadmap for the safe integration of generalist medical AI into clinical workflows.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 2","pages":"Pages 99-116"},"PeriodicalIF":7.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148378321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From “shooting in the dark” to “precision hit”: Technological evolution, synergistic strategies, and future paths for peripheral pulmonary nodule diagnosis","authors":"Ximing Liao,&nbsp;Qiang Li,&nbsp;Ko-pen Wang","doi":"10.1016/j.pccm.2026.03.001","DOIUrl":"10.1016/j.pccm.2026.03.001","url":null,"abstract":"","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 2","pages":"Pages 95-98"},"PeriodicalIF":7.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148378243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UBE2M deficiency in alveolar macrophages promotes emphysema through HIF-2α/MMP12 axis","authors":"Zhouyang Li,&nbsp;Dongyu Guo,&nbsp;Yong Wang,&nbsp;Haipin Chen,&nbsp;Na Li,&nbsp;Lingling Dong,&nbsp;Xuchen Xu,&nbsp;Yongchao Zhao,&nbsp;Yi Sun,&nbsp;Songmin Ying,&nbsp;Wen Li,&nbsp;Jiesen Zhou,&nbsp;Zhihua Chen","doi":"10.1016/j.pccm.2026.05.004","DOIUrl":"10.1016/j.pccm.2026.05.004","url":null,"abstract":"<div><h3>Background</h3><div>Chronic obstructive pulmonary disease (COPD) is a leading cause of global mortality; however, its pathogenesis remains incompletely understood, limiting therapeutic options. Protein neddylation, a key post-translational modification, has been implicated in chronic inflammatory diseases, but its role in COPD remains largely unexplored. Therefore, this study aims to investigate the role of protein neddylation in the pathogenesis of COPD and to explore its potential as a novel therapeutic target.</div></div><div><h3>Methods</h3><div>We assessed the neddylation pathway in macrophages from patients with COPD and from mice exposed to cigarette smoke (CS). Myeloid-specific ubiquitin-conjugating enzyme E2 M (<em>Ube2m</em>) knockout (UBE2M-conditional knockout [cKO]) mice were generated to investigate the causal role of UBE2M in emphysema. Cell-type specificity was confirmed using club cell-specific knockout (CC10-TetOn-Flox [CTF]-UBE2M) and myeloid-specific ubiquitin-conjugating enzyme E2 F (<em>Ube2f</em>) knockout (UBE2F-cKO) mice. Transcriptomic profiling, molecular biology techniques, and pharmacological inhibition were employed to delineate the underlying mechanisms.</div></div><div><h3>Results</h3><div>Alveolar macrophages from COPD patients and CS-exposed mice exhibited significant downregulation of UBE2M. UBE2M-cKO was sufficient to induce spontaneous emphysema, characterized by increased lung volume, alveolar destruction, and impaired lung function, and it exacerbated CS-induced lung injury. This phenotype was specific to myeloid UBE2M-cKO, as neither CTF-UBE2M nor UBE2F-cKO recapitulated the disease. Transcriptomic profiling of UBE2M-cKO macrophages identified matrix metalloproteinase 12 (<em>Mmp12</em>) as a key mediator of the emphysema phenotype, given its macrophage-specific expression and potent elastin-degrading function. Mechanistically, UBE2M deficiency led to the stabilization of hypoxia-inducible factor-2α (HIF-2α, encoded by <em>Epas1</em>), a known neddylation substrate, resulting in transcriptional upregulation of <em>Mmp12</em>. The HIF-2α inhibitor PT2385 attenuated <em>Mmp12</em> upregulation, and double knockout of <em>Ube2m</em> and <em>Epas1</em> (UBE2M-EPAS1-DKO) significantly ameliorated emphysema development.</div></div><div><h3>Conclusion</h3><div>Our study identifies UBE2M as a critical protector against emphysema by promoting HIF-2α degradation, thereby suppressing MMP12 expression. The UBE2M–HIF-2α–MMP12 axis represents a novel and specific pathogenic pathway in COPD, offering promising therapeutic targets.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 2","pages":"Pages 171-183"},"PeriodicalIF":7.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148378324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian rhythms and lung cancer biology and immunotherapy: Emerging opportunities and challenges","authors":"Fang Tian,&nbsp;Songkai Wang,&nbsp;Zhe Huang,&nbsp;Zhaohui Ruan,&nbsp;Jiacheng Dai,&nbsp;Huan Yan,&nbsp;Jiao Huang,&nbsp;Dan Yang,&nbsp;Xiaomei Li,&nbsp;Liang Zeng,&nbsp;Qinqin Xu,&nbsp;Yongchang Zhang","doi":"10.1016/j.pccm.2026.04.001","DOIUrl":"10.1016/j.pccm.2026.04.001","url":null,"abstract":"<div><div>The circadian rhythm is an intrinsic timekeeping system that precisely regulates a wide range of physiological and pathological processes. Its core molecular mechanisms and regulatory networks are gaining increasing attention in the field of lung cancer research. Substantial evidence indicates that circadian clock genes are not only deeply involved in lung cancer initiation and progression but also profoundly influence the dynamic remodeling of the tumor immune microenvironment (TIME) in lung cancer. This review summarizes the expression patterns and functional mechanisms of circadian clock genes in various cancers. It specifically elaborates on their regulatory roles in immune cell function, malignant behaviors of tumor cells, and interactions with stromal cells. The review also details how circadian disruption drives lung cancer development, progression, and immune evasion. Besides, we explore the potential impact of heterogeneity in circadian gene expression on the efficacy of immune checkpoint inhibitors (ICIs) in lung cancer, synthesize current knowledge on how circadian rhythms influence clinical responses to and adverse effects of immunotherapy in lung cancer, and highlight the translational potential of chronotherapy—optimizing drug administration timing based on circadian principles—to enhance therapeutic outcomes and reduce toxicity. By integrating recent preclinical and clinical evidence, this review provides a theoretical foundation for circadian-based precision immunotherapy in lung cancer and outlines future directions for innovative therapeutic strategies targeting the circadian machinery.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 2","pages":"Pages 137-154"},"PeriodicalIF":7.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148378313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanisms and therapeutic targets in lung cancer–nerve crosstalk","authors":"Ziyang Xu,&nbsp;Shanshan Huang,&nbsp;Qian Chu","doi":"10.1016/j.pccm.2026.05.003","DOIUrl":"10.1016/j.pccm.2026.05.003","url":null,"abstract":"<div><div>Reciprocal crosstalk between the nervous system and malignancies is increasingly recognized as a key regulator of tumor progression across solid cancers. Neuronal activity and nerve infiltration can shape tumor growth, immune tone, and metastatic behavior through paracrine signaling and, in selected contexts, synapse-like interactions. However, how neural circuits regulate lung cancer progression remains insufficiently defined. β-adrenergic blockade has been reported to be associated with reduced lung tumor growth and metastatic potential in multiple settings, highlighting the clinical relevance of innervation. Here we synthesize emerging evidence on lung cancer–nerve crosstalk from the perspective of cancer neuroscience, focusing on neural remodeling in the tumor microenvironment, mechanisms underlying tumorigenesis and metastasis, the neuro–immune–tumor axis, and translational opportunities for neuro-modulatory interventions. This review provides an integrated framework to inform future mechanistic studies and the development of therapeutically actionable targets.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 2","pages":"Pages 117-136"},"PeriodicalIF":7.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13323558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148378319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanovaccines for lung cancer: Platforms, mechanistic insights, and translational challenges","authors":"Hamed Hosseinalizadeh ,&nbsp;Fujing Ge ,&nbsp;Mohsen Davari ,&nbsp;Xiaohong Liu ,&nbsp;Lei Tian ,&nbsp;Jianhua Yu","doi":"10.1016/j.pccm.2026.02.001","DOIUrl":"10.1016/j.pccm.2026.02.001","url":null,"abstract":"<div><div>Lung cancer remains a global health challenge, with high mortality rates and frequent resistance to conventional therapies. In recent years, nanovaccines-based immunotherapy has emerged as a promising frontier, harnessing advances in nanotechnology to enable precise delivery of tumor-associated antigens, potentiate immune activation, and overcome barriers imposed by the tumor microenvironment. This review synthesizes current knowledge and recent progress in the field, highlighting several nanovaccine platforms from mRNA and protein constructs to biomimetic designs, which have demonstrated preclinical efficacy against both primary and metastatic lung cancer. We illustrate how innovations can elicit robust polyclonal T cell responses and remodel the immune landscape within tumors, including co-delivery of antigens and adjuvants, use of patient-derived materials, and integration of multi-omics. Furthermore, the combination of nanovaccines with current therapies, including immune checkpoint inhibitors, cell-based therapies, and gene-modulating strategies, offers new avenues for enhancing therapeutic outcomes. Despite these advances, several challenges remain, including barriers of large-scale manufacturing, safety assessment, regulatory approval, and the need for personalized optimization. Ongoing research and clinical studies will be essential to translate these experimental successes into personalized treatments for patients with lung cancer. Nanovaccine immunotherapy stands poised to become a transformative component in the evolving landscape of lung cancer management.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 1","pages":"Pages 1-18"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147556973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunotherapy for patients with EGFR-TKI-resistant non-small-cell lung cancer: Potential mechanisms, efficacy predictors, and therapeutic integration","authors":"Xinwei Wu ,&nbsp;Yangbin Shi ,&nbsp;Danni Wang ,&nbsp;Beibei Liu ,&nbsp;Yanwei Zhang ,&nbsp;Lele Zhang ,&nbsp;Fangfei Qian ,&nbsp;Wei Zhang","doi":"10.1016/j.pccm.2026.02.005","DOIUrl":"10.1016/j.pccm.2026.02.005","url":null,"abstract":"<div><div>Immunotherapy has revolutionized the treatment landscape of advanced non-small-cell lung cancer (NSCLC). However, its efficacy in patients with epidermal growth factor receptor (<em>EGFR</em>)-mutant NSCLC, particularly after failure of EGFR-tyrosine kinase inhibitors (TKIs), remains unclear and highly heterogeneous across individuals. This difference in treatment response is closely associated with the dynamic remodeling of the tumor microenvironment (TME) driven by the selective pressure of EGFR-TKIs. This review outlines the evolution of the TME during EGFR-TKI treatment and after the development of TKI resistance. Additionally, it summarizes current clinical evidence regarding immunotherapy after EGFR-TKI resistance, and discusses predictive biomarkers and novel therapeutic approaches. By integrating mechanistic insights with clinical translation, this review provides a comprehensive perspective on the immunotherapy landscape after TKI failure, aiming to identify patient subgroups most likely to benefit from immunotherapy and optimize treatment strategies for <em>EGFR</em>-mutant NSCLC.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 1","pages":"Pages 61-71"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147556968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asthma endotypes and theratypes","authors":"Ioana Agache ,&nbsp;Shengjie Li ,&nbsp;Yang Zheng ,&nbsp;Yadong Gao","doi":"10.1016/j.pccm.2026.02.006","DOIUrl":"10.1016/j.pccm.2026.02.006","url":null,"abstract":"<div><div>The model of asthma as a single entity has now been replaced by a much more complex biological network of distinct and interrelating inflammatory and tissue driven pathways. Individual disease manifestations (phenotypes), pathogenetic pathways (endotypes) and response to therapy (theratypes) are discussed here in the context of current stratified management of asthma in the clinic based on biomarkers measured at the point-of-care. As the current classification criteria result in significant overlaps among phenotypes, endotypes and theratypes, this paper further describes the advantage of combining precision immunology, imaging and the digital biomarkers in an unbiased approach offered by machine learning. The new European Academy of Allergy and Clinical Immunology (EAACI) nomenclature for hypersensitivity reaction is detailed as a basis for the stratified asthma management with a special focus on tissue-driven mechanisms (type V asthma), metabolic/microbiome/epigenetic/neurogenic mechanisms (type VI asthma) and direct cellular activation (type VII asthma).</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 1","pages":"Pages 19-38"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147556969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progression of interstitial lung abnormalities and its impact on mortality in patients with lung cancer resection","authors":"Ruolin Mao ,&nbsp;Haoyun Zhang ,&nbsp;Qing Chang ,&nbsp;Yilong Teng ,&nbsp;Yanfen Ni ,&nbsp;Jiani Chen ,&nbsp;Mengnan Li ,&nbsp;Ning Xu ,&nbsp;Hai Zhang ,&nbsp;Yuqing Chen ,&nbsp;Jianqi Sun ,&nbsp;Kian Fan Chung ,&nbsp;Elisabetta A. Renzoni ,&nbsp;Yi Lu ,&nbsp;Huaping Dai ,&nbsp;Feng Li","doi":"10.1016/j.pccm.2026.02.004","DOIUrl":"10.1016/j.pccm.2026.02.004","url":null,"abstract":"<div><h3>Background</h3><div>Interstitial lung abnormalities (ILAs) are incidental abnormal lung findings on computed tomography that can co-exist with lung cancer, but risk factors for their progression and impact on survival after lung cancer resection remain unclear. This study aimed to identify risk factors for ILA progression, develop a radiomics-based model to predict it, and evaluate the association between ILA progression and mortality.</div></div><div><h3>Methods</h3><div>Patients with ILAs who underwent lung cancer resection in Shanghai Chest Hospital between January 2016 and May 2019 were retrospectively selected and divided into three subcategories at baseline: non-subpleural ILAs, subpleural non-fibrotic ILAs, and subpleural fibrotic ILAs; and three subcategories during follow-up: improved ILAs, unchanged ILAs, and progressive ILAs. Multivariate logistic regression was used to identify clinical and laboratory risk factors associated with ILA progression, and radiomics-based machine learning models were independently constructed to predict ILA progression using baseline CT imaging features. Survival data were analyzed using Kaplan–Meier curves and Cox proportional hazards regression.</div></div><div><h3>Results</h3><div>There were 1363 ILA cases among 10,295 patients who underwent primary lung cancer resection, with a proportion of 13.24%. After 2- and 4-year follow-up, the progression rates of ILAs were 9.86% (65/659) and 10.19% (43/422), respectively. Subpleural fibrotic ILAs (2-year follow-up: OR = 6.078, 95% confidence interval [CI]: 2.633–14.028, <em>P</em> &lt; 0.001; 4-year follow-up: OR = 3.339, 95% CI: 1.085–10.272, <em>P</em> = 0.035), and radiotherapy (OR = 13.595, 95% CI: 4.540–40.710, <em>P</em> &lt; 0.001; OR = 11.496, 95% CI: 2.864–46.141, <em>P</em> = 0.001) were risk factors for ILA progression. Using radiomics features extracted from baseline CT, the AutoGluon machine learning model demonstrated high performance in predicting ILA progression among patients with confirmed ILAs (for all ILAs, mean area under curve value: 0.790, accuracy: 0.801 ± 0.049). The all-cause mortality rates at 2- and 4-year follow-up were 2.11% (27/1281) and 4.26% (53/1245), respectively. Both subpleural fibrotic (log-rank <em>χ</em>² = 23.910, <em>P</em> &lt; 0.001) and progressive ILA groups (log-rank <em>χ</em>² = 26.098, <em>P</em> &lt; 0.001) had higher mortality rates compared with non-subpleural, subpleural non-fibrotic ILA group and improved, unchanged ILA group; and progressive ILAs were a risk factor for death (HR = 2.824, 95% CI: 1.065–7.483, <em>P</em> = 0.037).</div></div><div><h3>Conclusions</h3><div>ILA progression occurs in about 10% of patients after lung cancer resection and is associated with higher mortality. Subpleural fibrotic ILAs and radiotherapy are key risk factors for progression. Radiomics features effectively predict ILA progression, enabling early identification of high-risk patients.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 1","pages":"Pages 81-91"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147556971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incidence of acute exacerbation and its related factors among chronic obstructive pulmonary disease patients aged 40 years and older in China","authors":"Qi Luo,&nbsp;Shu Cong,&nbsp;Shige Qi,&nbsp;Jing Fan,&nbsp;Wenjing Wang,&nbsp;Xueting Wang,&nbsp;Liwen Fang","doi":"10.1016/j.pccm.2026.02.002","DOIUrl":"10.1016/j.pccm.2026.02.002","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Acute exacerbation of chronic obstructive pulmonary disease (COPD) (AECOPD) represents a pivotal event in the clinical course of COPD and contributes substantially to disease progression and healthcare burden. This study examined the incidence and demographic distribution of AECOPD among Chinese COPD patients aged ≥40 years and evaluated factors associated with its occurrence, providing population-based evidence to inform community prevention, standardized treatment, rehabilitation, and health management strategies.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Data were derived from the Chinese Chronic Obstructive Pulmonary Disease Surveillance (2019–2020), a nationwide cross-sectional survey conducted in 125 surveillance counties (districts) across 31 provinces, autonomous regions, and municipalities in China. Using a multistage stratified cluster random sampling design, residents aged ≥40 years were enrolled. Participants completed standardized questionnaires, physical measurements, and pre- and post-bronchodilator spirometry administered by trained investigators. COPD was defined as a post-bronchodilator forced expiratory volume in one second (FEV₁)/forced vital capacity (FVC) &lt;70%. The incidence of AECOPD and corresponding hospitalization rates were estimated and compared across subgroups. Stepwise multivariable logistic regression was used to identify factors associated with AECOPD, with Model I including sociodemographic, behavioral, and environmental factors and Model II additionally incorporating disease-related characteristics.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;A total of 7455 COPD patients were included in the analysis. The overall incidence of AECOPD was 9.0% (95% confidence interval [CI]: 7.9–10.1%), and the hospitalization rate was 4.3% (95% CI: 3.5–5.0%). Higher incidence and hospitalization rates were observed among patients aged ≥65 years (10.8%, 5.7%) and those residing in southern region (10.3%, 5.0%). Elevated rates were also noted among individuals with body mass index (BMI) &lt;18.5 kg/m² (16.1%, 10.0%), smoking history (9.1%, 4.3%), prior hospital admission for severe pulmonary disease in childhood (21.6%, 9.3%), exposure to biomass (10.8%, 5.3%), occupational exposure to harmful factors (10.5%, 4.9%), and a history of chronic respiratory diseases (28.2%, 14.9%). The highest rates were observed in patients with a modified Medical Research Council (mMRC) score ≥2 (40.7%, 23.0%). Rates were 22.4% and 11.5% among those with a COPD Assessment Test (CAT) score ≥10 and 33.0% and 19.5% among those with ≥3 comorbidities. By Global Initiative for Chronic Obstructive Lung Disease (GOLD) grades, incidence and hospitalization rates were 4.6% and 1.7% (Stage I), 10.7% and 4.6% (Stage II), and 28.7% and 18.9% (Stages III–IV). Multivariable analyses identified residence in southern region, hospital admission for severe pulmonary disease in childhood, mMRC score ≥2, CAT score ≥10, GOLD stage III–IV, and a higher n","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"4 1","pages":"Pages 72-80"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147556972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}