109906
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.4 Breast Cancer (Dove Med Press)
- 3.2 Clin Epidemiol
- 2.6 Cancer Manag Res
- 2.9 Infect Drug Resist
- 3.7 Clin Interv Aging
- 5.1 Drug Des Dev Ther
- 3.1 Int J Chronic Obstr
- 6.6 Int J Nanomed
- 2.6 Int J Women's Health
- 2.9 Neuropsych Dis Treat
- 2.8 OncoTargets Ther
- 2.0 Patient Prefer Adher
- 2.2 Ther Clin Risk Manag
- 2.5 J Pain Res
- 3.0 Diabet Metab Synd Ob
- 3.2 Psychol Res Behav Ma
- 3.4 Nat Sci Sleep
- 1.8 Pharmgenomics Pers Med
- 2.0 Risk Manag Healthc Policy
- 4.1 J Inflamm Res
- 2.0 Int J Gen Med
- 3.4 J Hepatocell Carcinoma
- 3.0 J Asthma Allergy
- 2.2 Clin Cosmet Investig Dermatol
- 2.4 J Multidiscip Healthc
已发表论文
巨噬细胞抗结核分枝杆菌感染的葡萄糖代谢重编程
Authors Liu T, Yang Z, Tong J, Gao M, Pang Y
Received 10 July 2025
Accepted for publication 16 October 2025
Published 31 October 2025 Volume 2025:14 Pages 1209—1221
DOI https://doi.org/10.2147/ITT.S552746
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Sarah Wheeler
Tianhui Liu,1,* Zeliang Yang,2,* Jing Tong,1 Mengqiu Gao,1 Yu Pang2
1Department of Tuberculosis II, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, People’s Republic of China; 2Department of Bacteriology and Immunology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Mengqiu Gao, Department of Tuberculosis II, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, People’s Republic of China, Email gaomqwdm@aliyun.com Yu Pang, Department of Bacteriology and Immunology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, People’s Republic of China, Email pangyupound@163.com
Abstract: Tuberculosis (TB) is a global infectious disease caused by Mycobacterium tuberculosis (Mtb). Serving as the primary effector cells, macrophages play a crucial role in host immune responses against Mtb. During Mtb infection, macrophages undergo extensive metabolic reprogramming, notably glycolysis, the pentose phosphate pathway (PPP) and the tricarboxylic acid (TCA) cycle, to adapt to the challenges posed by the pathogen, with glucose metabolic rewiring being particularly critical. This review focuses on the dynamic reprogramming of glucose metabolism in macrophages during Mtb infection, highlighting how metabolic adjustments influence the activation state, polarization, and functional capacity of macrophages. Furthermore, we explore the role of glucose metabolic reprogramming in shaping the immune responses against Mtb, particularly its contribution to granuloma formation and maintenance. By understanding the intricate interplay between metabolic rewiring and immune function, we discuss the therapeutic potential of targeting glucose metabolic pathways in macrophages as a novel strategy for TB treatment. Overall, this review emphasizes the need for a deeper understanding of the relationship between glucose metabolism reprogramming and the biological function of Mtb-infected macrophages and the development of novel immunometabolic therapies—such as metformin (AMPK activator) or PKM2 modulators already used in oncology— to improve the outcomes of TB patients.
Keywords: glucose metabolic reprogramming, macrophages, Mycobacterium tuberculosis
1Department of Tuberculosis II, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, People’s Republic of China; 2Department of Bacteriology and Immunology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Mengqiu Gao, Department of Tuberculosis II, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, People’s Republic of China, Email gaomqwdm@aliyun.com Yu Pang, Department of Bacteriology and Immunology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, People’s Republic of China, Email pangyupound@163.com
Abstract: Tuberculosis (TB) is a global infectious disease caused by Mycobacterium tuberculosis (Mtb). Serving as the primary effector cells, macrophages play a crucial role in host immune responses against Mtb. During Mtb infection, macrophages undergo extensive metabolic reprogramming, notably glycolysis, the pentose phosphate pathway (PPP) and the tricarboxylic acid (TCA) cycle, to adapt to the challenges posed by the pathogen, with glucose metabolic rewiring being particularly critical. This review focuses on the dynamic reprogramming of glucose metabolism in macrophages during Mtb infection, highlighting how metabolic adjustments influence the activation state, polarization, and functional capacity of macrophages. Furthermore, we explore the role of glucose metabolic reprogramming in shaping the immune responses against Mtb, particularly its contribution to granuloma formation and maintenance. By understanding the intricate interplay between metabolic rewiring and immune function, we discuss the therapeutic potential of targeting glucose metabolic pathways in macrophages as a novel strategy for TB treatment. Overall, this review emphasizes the need for a deeper understanding of the relationship between glucose metabolism reprogramming and the biological function of Mtb-infected macrophages and the development of novel immunometabolic therapies—such as metformin (AMPK activator) or PKM2 modulators already used in oncology— to improve the outcomes of TB patients.
Keywords: glucose metabolic reprogramming, macrophages, Mycobacterium tuberculosis