<?xml version="1.1" encoding="utf-8"?>
<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">MRP</journal-id><journal-title-group><journal-title>Medical Research and Practice</journal-title></journal-title-group><issn>2993-9690</issn><eissn>2993-9704</eissn><publisher><publisher-name>Art and Technology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.61369/MRP.2026030009</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>慢性阻塞性肺疾病合并肺癌研究进展
—— 共同危险因素及发病机制</title><url>https://artdesignp.com/journal/MRP/4/3/10.61369/MRP.2026030009</url><author>卢倩倩,李丽</author><pub-date pub-type="publication-year"><year>2026</year></pub-date><volume>4</volume><issue>3</issue><history><date date-type="pub"><published-time>2026-03-20</published-time></date></history><abstract>慢性阻塞性肺疾病（chronic obstructive pulmonary disease, COPD）和肺癌是世界范围内导致死亡的疾病之一，给全球带来了沉重社会和经济负担。COPD和肺癌的共病高发提示二者可能存在共同的危险因素和发病机制。其中吸烟、环境空气污染是二者共同的危险因素。越来越多的证据显示，慢性炎症、遗传易感性、表观遗传、端粒长度、慢性炎症、氧化应激反应和肺部微生物等是COPD和肺癌发生发展的共同通路。本文就COPD合并肺癌的主要危险因素及共同发病机制作一综述，为疾病早期早期筛查、诊断及治疗策略提供依据。</abstract><keywords>肺癌,慢性阻塞性肺疾病,慢性阻塞性肺疾病合并肺癌,危险因素,共同发病机制</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[1]Zeneyedpour L, Dekker L, van Sten-van T H J, et al. Neoantigens in Chronic Obstructive Pulmonary Disease and Lung Cancer: A Point of View[J]. Proteomics Clin Appl,2019,13(2):e1800093.DOI:10.1002/prca.201800093.[2] 肖雄, 许毅娇, 陈志盛, 等. 慢性阻塞性肺疾病患者肺泡灌洗液宏基因组测序分析[J]. 中国病原生物学杂志, 2022,17(10):1188-1191.DOI:10.13350/j.cjpb.221016.[3] 吴漫, 吴健卫, 徐非洲, 等. 慢性阻塞性肺疾病合并肺癌现状调查及预后初探[J]. 临床肺科杂志, 2025,30(2):219-225.DOI:10.3969/j.issn.1009-6663.2025.02.010.[4]Siegel R L, Giaquinto A N, Jemal A. Cancer statistics, 2024[J]. CA: A Cancer Journal for Clinicians, 2024,74(1):12-49.DOI:10.3322/caac.21820.[5]Forder A, Zhuang R, Souza V G P, et al. Mechanisms Contributing to the Comorbidity of COPD and Lung Cancer[J]. International journal of molecular sciences,2023,24(3):2859.DOI:10.3390/ijms24032859.[6] 吴漫, 徐兴祥. 慢性阻塞性肺疾病合并肺癌的研究进展[J]. 中华肺部疾病杂志( 电子版), 2019,12(05):646-649.[7]魏沛, 魏玉娟. 西安市慢性阻塞性肺疾病流行现状、趋势及影响因素分析_ 魏沛[J]. 中国社会医学杂志, 2022.[8]Wang K, Li J, Zhang H, et al. Tobacco Smoking Rewires Cell Metabolism by Inducing GAPDH Succinylation to Promote Lung Cancer Progression[J]. Cancer Res, 2025.DOI:10.1158/0008-5472.CAN-24-3525.[9] 秦佳玉, 霍建民. 空气污染对气流阻塞性疾病的影响[J]. 临床肺科杂志, 2019,24(1):159-162.DOI:10.3969/j.issn.1009-6663.2019.01.040.[10]Wang Y, Jin L, Dong Y, et al. Global burden of disease study on COPD in the older adult: comprehensive analysis of environmental factors and interaction effects[J].Frontiers in Public Health, 2025,13:1597793.DOI:10.3389/fpubh.2025.1597793.[11]Wen J, Yang Y, Zhang H, et al. PM2.5 increases the risk of early-onset COPD mediated by smoking and shared genes: a large-scale genetic analysis[J]. Clinical and Experimental Medicine, 2025,25(1):116.DOI:10.1007/s10238-025-01644-9.[12]Jin T, Lee S, Seo J, et al. Long-term ambient ozone exposure and lung cancer mortality: A nested case-control study in Korea[J]. Environmental Pollution, 2025,375:126299.DOI:https://doi.org/10.1016/j.envpol.2025.126299.[13]Cochard M, Ledoux F, And Landkocz Y. Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies[J]. Journal of Toxicology and Environmental Health, Part B, 2020,23(7):293-318.DOI:10.1080/10937404.2020.1816238.[14] 林慧, 余其梅, 付国庆, 等. 黑碳与炭黑颗粒对呼吸系统影响的异同与研究展望[J]. 环境与健康杂志, 2019,36(10):852-856.DOI:10.16241/j.cnki.1001-5914.2019.10.002.[15]&amp;Scaron;ileikienė V, Jurgauskienė L. Role of Regulatory T Cells in Pulmonary Ageing and COPD Development[J]. International Journal of Molecular Sciences, 2025,26(8):3721.DOI:10.3390/ijms26083721.[16] 余中杰, 高阳. 慢性阻塞性肺疾病与肺癌：共病机制及综合管理策略[J]. 中国现代医学杂志, 2025,35(08):38-44.[17]Ahmadi A, Ahrari S, Salimian J, et al. p38 MAPK signaling in chronic obstructive pulmonary disease pathogenesis and inhibitor therapeutics.[J]. Cell communication and signaling : CCS, 2023,21(1):314.DOI:10.1186/s12964-023-01337-4.[18]Forder A, Zhuang R, Souza V G P, et al. Mechanisms Contributing to the Comorbidity of COPD and Lung Cancer.LID - 10.3390/ijms24032859 [doi]LID - 2859[J]. International journal of molecular sciences, 2023,24(3).DOI:10.3390/ijms24032859.
[19]Thai H, Hassanen R, Whittall T, et al. The potential role of 1,25(OH)2D3 (Active vitamin D3) in modulating macrophage function; implications for chronic obstructive pulmonary disease (COPD)[J]. Journal of Inflammation, 2025,22(1):26.DOI:10.1186/s12950-025-00452-y.[20]Qi C, Sun S W, Xiong X Z. From COPD to Lung Cancer: Mechanisms Linking, Diagnosis, Treatment, and Prognosis[J]. Int J Chron Obstruct Pulmon Dis, 2022,17:2603-2621.DOI:10.2147/COPD.S380732.[21]Wan A, Chen D. The Multifaceted Roles of Neutrophil Death in COPD and Lung Cancer[J]. Journal of Respiratory Biology and Translational Medicine, 2024,1(4):10022.DOI:10.70322/jrbtm.2024.10022.[22]Kaltenmeier C, Yazdani H O, Morder K, et al. Neutrophil Extracellular Traps Promote T Cell Exhaustion in the Tumor Microenvironment[J]. Frontiers in Immunology, 2021,12:785222.DOI:10.3389/fimmu.2021.785222.[23]Xia H, Wu Y, Zhao J, et al. N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2.[J].Cell death and differentiation, 2023,30(5):1293-1304.DOI:10.1038/s41418-023-01138-9.[24]Yoshida M, Minagawa S, Araya J, et al. Involvement of cigarette smoke-induced epithelial cell ferroptosis in COPD pathogenesis.[J]. Nature communications, 2019,10(1):3145.DOI:10.1038/s41467-019-10991-7.[25]Xu Y, Lv D, Yan C, et al. METTL3 promotes lung adenocarcinoma tumor growth and inhibits ferroptosis by stabilizing SLC7A11 m(6)A modification.[J]. Cancer cell international, 2022,22(1):11.DOI:10.1186/s12935-021-02433-6.[26]Li Q, Song Q, Pei H, et al. Emerging mechanisms of ferroptosis and its implications in lung cancer.[J]. Chinese medical journal, 2024,137(7):818-829.DOI:10.1097/CM9.0000000000003048.[27]Yang L, Yang Z, Zuo C, et al. Epidemiological evidence for associations between variants in CHRNA genes and risk of lung cancer and chronic obstructive pulmonary disease[J]. Frontiers in Oncology, 2022,12:1001864.DOI:10.3389/fonc.2022.1001864.[28]Fujimoto J, Nunomura Nakamura S, Liu Y, et al. Development ofKras mutant lung adenocarcinoma in mice with knockout of the airway lineage ‐specific geneG prc5a[J]. International Journal of Cancer, 2017,141(8):1589-1599.DOI:10.1002/ijc.30851.[29]Tessema M, Yingling C M, Picchi M A, et al. Epigenetic Repression of CCDC37 and MAP1B Links Chronic Obstructive Pulmonary Disease to Lung Cancer.[J]. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2015,10(8):1181-1188.DOI:10.1097/JTO.0000000000000592.[30]Tessema M, Tassew D D, Yingling C M, et al. Identification of novel epigenetic abnormalities as sputum biomarkers for lung cancer risk among smokers and COPD patients[J]. Lung Cancer, 2020,146:189-196.DOI:10.1016/j.lungcan.2020.05.017.[31]Bojesen S E, Timpson N, Relton C, et al. AHRR (cg05575921) hypomethylation marks smoking behaviour, morbidity and mortality.[J]. Thorax, 2017,72(7):646-653. DOI:10.1136/thoraxjnl-2016-208789.[32]Mirra D, Esposito R, Spaziano G, et al. MicroRNA Monitoring in Human Alveolar Macrophages from Patients with Smoking-Related Lung Diseases: A Preliminary Study. LID - 10.3390/biomedicines12051050 [doi]LID - 1050[J]. Biomedicines, 2024,12(5).DOI:10.3390/biomedicines12051050.[33]C&amp;oacute;rdoba-Lan&amp;uacute;s E, Dom&amp;iacute;nguez De-Barros A, Oliva A, et al. Circulating miR-206 and miR-1246 as Markers in the Early Diagnosis of Lung Cancer in Patients with Chronic Obstructive Pulmonary Disease[J]. International Journal of Molecular Sciences, 2023,24(15):12437.DOI:10.3390/ijms241512437.[34]Mirra D, Esposito R, Spaziano G, et al. Lung microRNAs Expression in Lung Cancer and COPD: A Preliminary Study.LID - 10.3390/biomedicines11030736 [doi] LID -736[J]. Biomedicines, 2023,11(3).DOI:10.3390/biomedicines11030736.[35]Rivas M, Gupta G, Costanzo L, et al. Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease.LID - 10.3390/medicina58060817 [doi]LID - 817[J]. Medicina (Kaunas, Lithuania), 2022,58(6).DOI:10.3390/medicina58060817.[36]Tsatsakis A, Oikonomopoulou T, Nikolouzakis T K, et al. Role of telomere length in human carcinogenesis (Review).LID - 78 [pii]LID - 10.3892/ijo.2023.5526 [doi][J]. International journal of oncology, 2023,63(1).DOI:10.3892/ijo.2023.5526.[37]Wang T, Su W, Li L, et al. Alteration of the gut microbiota in patients with lung cancer accompanied by chronic obstructive pulmonary diseases.[J]. Heliyon,2024,10(9):e30380.DOI:10.1016/j.heliyon.2024.e30380.[38] 木亚莎尔&amp;middot; 吐逊江, 王雨琳, 曹洪丽. 慢性阻塞性肺疾病合并肺癌共同发病机制[J]. 中国组织化学与细胞化学杂志, 2022,31(04):412-416.DOI:10.16705/j.cnki.1004-1850.2022.04.014.[39]Jiang H, Huang G, Feng D, et al. Comorbidity of lung cancer and chronic obstructive pulmonary disease: correlation and optimization of treatment strategies.[J]. Translational lung cancer research, 2025,14(6):2296-2308.DOI:10.21037/tlcr-2025-480.[40]Zhou J, Hou W, Zhong H, et al. Lung microbiota: implications and interactions in chronic pulmonary diseases.[J]. Frontiers in cellular and infection microbiology,2024,14:1401448.DOI:10.3389/fcimb.2024.1401448.[41]Cheng J, Zhou L, Wang H. Symbiotic microbial communities in various locations of the lung cancer respiratory tract along with potential host immunological processes affected[J]. Frontiers in Cellular and Infection Microbiology,2024,14:1296295.DOI:10.3389/fcimb.2024.1296295.</p><pub-id pub-id-type="doi"/></element-citation></ref></ref-list></back></article>
