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哮喘发病机制中糖酵解的研究进展
Received 18 March 2025
Accepted for publication 3 July 2025
Published 26 July 2025 Volume 2025:18 Pages 1147—1160
DOI https://doi.org/10.2147/JAA.S528965
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Luis Garcia-Marcos
Jindan Luo,1 Xiaoli Ge1,2
1Department of Pediatrics, The Affiliated Wuxi Second Hospital of Nanjing Medical University, Wuxi, 214000, People’s Republic of China; 2Department of Pediatrics, The Affiliated Wuxi Second People’s Hospital of Jiangnan University, Wuxi, 214000, People’s Republic of China
Correspondence: Xiaoli Ge, Department of Pediatrics, The Affiliated Wuxi Second Hospital of Nanjing Medical University, No. 68 of Zhongshan Road, Wuxi, 214000, People’s Republic of China, Tel +86-15936078575, Email gexiaolidrgxl@163.com
Abstract: Asthma is a chronic, complex, and heterogeneous respiratory condition marked by airway hyperresponsiveness and reversible airflow limitation. Recent evidence highlights the significant role of metabolic changes, particularly glycolytic reprogramming, in the pathogenesis of asthma. Glycolysis, a fundamental pathway for both anaerobic and aerobic oxidation, not only generates adenosine triphosphate (ATP) but also supplies substrates for lipid-based ATP storage. While initially studied in the context of cancer, glycolysis has been associated with asthma through its interplay with programmed cell death, which is crucial in asthma pathophysiology. This study offers a comprehensive overview of current research on glycolytic reprogramming in asthma, emphasizing its potential implications and significance. The findings aim to inform future studies and contribute to the development of asthma-related precision medicine. A deeper understanding of the interplay between glycolysis and the development and progression of asthma may facilitate the development of innovative therapeutic approaches for this complex condition.
Keywords: asthma, glycolysis, immune cells, precision medicine, programmed cell death