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已发表论文
慢性阻塞性肺疾病中吸烟诱导的葡萄糖代谢重编程：机制及治疗意义
Authors Ji T , Gu YY, Gao YM, Xie Y, Liu Z, Cheng A, Zhou X , Ailifeire A, Wang M, Song Q, Shi Y, Shi S, He J, Zhao L, Xiao D, Wang C
Received 28 July 2025
Accepted for publication 24 November 2025
Published 2 December 2025 Volume 2025:20 Pages 3855—3866
DOI https://doi.org/10.2147/COPD.S556362
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr Vanesa Bellou
Tingfen Ji,1– 6 Yang-Yang Gu,7 Ying-Man Gao,2– 6,8 Ying Xie,2– 6,8 Zhao Liu,2– 6 Anqi Cheng,2– 6 Xinmei Zhou,2– 6,9 Aihemaiti Ailifeire,2– 6,8 Min Wang,2– 6,8 Qingqing Song,1– 6 Yuxin Shi,2– 6,8 Shunyi Shi,2– 6,9 Jiahui He,1– 6 Liang Zhao,2– 6 Dan Xiao,2– 6,8 Chen Wang2– 6,8
1China-Japan Friendship School of Clinical Medicine, Capital Medical University, Beijing, People’s Republic of China; 2Department of Tobacco Control and Prevention of Respiratory Diseases, China-Japan Friendship Hospital, Beijing, People’s Republic of China; 3WHO Collaborating Center for Tobacco Cessation and Respiratory Diseases Prevention, Beijing, People’s Republic of China; 4National Clinical Research Center for Respiratory Diseases, Beijing, People’s Republic of China; 5Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China; 6National Center for Respiratory Medicine, Beijing, People’s Republic of China; 7Department of Respiratory & Critical Care Medicine, Jiaxing Second Hospital, The Second Affiliated Hospital of Jiaxing University, Jiaxing, People’s Republic of China; 8Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China; 9School of Health Policy and Management, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People’s Republic of China
Correspondence: Dan Xiao, Department of Tobacco Control and Prevention of Respiratory Diseases, China-Japan Friendship Hospital, No. 2 Yinghua East Street, Chaoyang District, Beijing, 100029, People’s Republic of China, Email danxiao@263.net
Abstract: Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous respiratory disorder that arises from interactions between genetic susceptibility and environmental exposures, with cigarette smoking being the primary modifiable risk factor. Cigarette smoke reprograms pulmonary glucose metabolism, a process recognized as an early molecular event driving disease progression. Prolonged exposure is associated with enhanced glycolysis, suppression of the tricarboxylic acid cycle and oxidative phosphorylation, mitochondrial dysfunction, and excessive production of mitochondrial reactive oxygen species. These metabolic disturbances converge to form a pathological axis linking metabolism, inflammation, and immunity, leading to immune dysregulation, chronic airway inflammation, and tissue remodeling. This review summarizes the characteristics and molecular mechanisms of cigarette smoke–induced glucose metabolic reprogramming in COPD while highlighting the therapeutic potential of targeting glucose metabolism. Particular emphasis is placed on comprehensive strategies aimed at restoring metabolic homeostasis. A deeper understanding of glucose metabolic reprogramming in COPD associated with smoking may provide novel insights into disease pathogenesis and contribute to the development of individualized therapies. Nevertheless, clinical evidence remains limited, underscoring the need for translational studies targeting glucose metabolism in COPD.
Keywords: chronic obstructive pulmonary disease, glucose metabolism reprogramming, cigarette smoke, mitochondrial dysfunction, targeted metabolic intervention
1China-Japan Friendship School of Clinical Medicine, Capital Medical University, Beijing, People’s Republic of China; 2Department of Tobacco Control and Prevention of Respiratory Diseases, China-Japan Friendship Hospital, Beijing, People’s Republic of China; 3WHO Collaborating Center for Tobacco Cessation and Respiratory Diseases Prevention, Beijing, People’s Republic of China; 4National Clinical Research Center for Respiratory Diseases, Beijing, People’s Republic of China; 5Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China; 6National Center for Respiratory Medicine, Beijing, People’s Republic of China; 7Department of Respiratory & Critical Care Medicine, Jiaxing Second Hospital, The Second Affiliated Hospital of Jiaxing University, Jiaxing, People’s Republic of China; 8Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China; 9School of Health Policy and Management, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People’s Republic of China
Correspondence: Dan Xiao, Department of Tobacco Control and Prevention of Respiratory Diseases, China-Japan Friendship Hospital, No. 2 Yinghua East Street, Chaoyang District, Beijing, 100029, People’s Republic of China, Email danxiao@263.net
Abstract: Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous respiratory disorder that arises from interactions between genetic susceptibility and environmental exposures, with cigarette smoking being the primary modifiable risk factor. Cigarette smoke reprograms pulmonary glucose metabolism, a process recognized as an early molecular event driving disease progression. Prolonged exposure is associated with enhanced glycolysis, suppression of the tricarboxylic acid cycle and oxidative phosphorylation, mitochondrial dysfunction, and excessive production of mitochondrial reactive oxygen species. These metabolic disturbances converge to form a pathological axis linking metabolism, inflammation, and immunity, leading to immune dysregulation, chronic airway inflammation, and tissue remodeling. This review summarizes the characteristics and molecular mechanisms of cigarette smoke–induced glucose metabolic reprogramming in COPD while highlighting the therapeutic potential of targeting glucose metabolism. Particular emphasis is placed on comprehensive strategies aimed at restoring metabolic homeostasis. A deeper understanding of glucose metabolic reprogramming in COPD associated with smoking may provide novel insights into disease pathogenesis and contribute to the development of individualized therapies. Nevertheless, clinical evidence remains limited, underscoring the need for translational studies targeting glucose metabolism in COPD.
Keywords: chronic obstructive pulmonary disease, glucose metabolism reprogramming, cigarette smoke, mitochondrial dysfunction, targeted metabolic intervention