糖酵解-乳酸化修饰在哮喘中的潜在作用与治疗展望

doi:10.12092/j.issn.1009-2501.2026.01.011

中国临床药理学与治疗学 ›› 2026, Vol. 31 ›› Issue (1): 96-106.doi: 10.12092/j.issn.1009-2501.2026.01.011

糖酵解-乳酸化修饰在哮喘中的潜在作用与治疗展望

沈小平¹^,²(), 吴东², 于丽丽¹^,³^,*(), 吴斌¹^,²^,*()

1. 中医药学院，医学部，澳门科技大学，澳门 999078
2. 广东医科大学附属医院呼吸与危重症医学科，湛江 524000，广东
3. 澳门科技大学珠海澳科大科技研究院，珠海 519099，广东

收稿日期:2025-07-15 修回日期:2025-09-18 出版日期:2026-01-26 发布日期:2026-02-13
通讯作者: 于丽丽,吴斌 E-mail:shenxp1985@163.com;llyu@must.edu.mo;wubin621011@126.com
作者简介:沈小平，男，在读博士研究生，主治医师，研究方向：中医药防治慢性气道炎症性疾病的基础和临床研究。E-mail：shenxp1985@163.com
基金资助:
广东省自然科学基金（2022A1515011731；2023A1515010410）

Potential role and therapeutic prospects of glycolysis-lactylation modification in asthma

Xiaoping SHEN¹^,²(), Dong WU², Lili YU¹^,³^,*(), Bin WU¹^,²^,*()

1. Faculty of Chinese Medicine, Medical Sciences Division, Macau University of Science and Technology, Macao 999078, China
2. Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524000, Guangdong, China
3. Macau University of Science and Technology Zhuhai MUST Science and Technology Research Institute, Zhuhai 519099, Guangdong, China

Received:2025-07-15 Revised:2025-09-18 Online:2026-01-26 Published:2026-02-13
Contact: Lili YU,Bin WU E-mail:shenxp1985@163.com;llyu@must.edu.mo;wubin621011@126.com

摘要/Abstract

摘要：

哮喘作为一种以气道慢性炎症、气道高反应性及重塑为特征的异质性疾病，其病理机制涉及多种免疫细胞与结构细胞的复杂交互作用。近年研究揭示，糖酵解与哮喘的发病机制、严重程度密切相关，各种免疫细胞中异常的糖酵解代谢可通过诱导先天性和适应性免疫反应失调来促进哮喘的发病机制。糖酵解终产物的乳酸直接介导了乳酸化修饰，进而调控表观遗传与信号通路，在Th2型炎症、巨噬细胞活化及气道重塑中发挥关键作用，可能成为哮喘病理进程中的潜在的调控节点。本综述讨论了糖酵解-乳酸化在哮喘中的潜在作用和机制，并分析靶向糖酵解-乳酸化通路作为哮喘治疗新策略的可能性，为未来的研究提供参考和方向。

关键词: 支气管哮喘, 慢性气道炎症, 糖酵解, 乳酸化, 代谢重编程

Abstract:

Asthma is a heterogeneous disease characterized by chronic airway inflammation, airway hyperresponsiveness, and remodeling. Its pathological mechanisms involve complex interactions between multiple immune and structural cells. Recent studies reveal that glycolysis is closely associated with the pathogenesis and severity of asthma. Dysregulated glycolytic metabolism in various immune cells promotes asthmatic pathogenesis by inducing dysfunctions in both innate and adaptive immune responses. Lactate, the end-product of glycolysis, directly mediates lactylation modifications that regulate epigenetic processes and signaling pathways. This mechanism plays critical roles in Th2 inflammation, macrophage activation, and airway remodeling, potentially serving as a regulatory hub in asthma pathology. In this review, we discuss the potential roles and mechanisms of glycolysis-lactylation in asthma, analyze the feasibility of targeting the glycolysis-lactylation axis as a novel therapeutic approach for asthma, and provide references and directions for future research.

Key words: bronchial asthma, chronic airway inflammation, glycolysis, lactylation, metabolic reprogramming

中图分类号:

R562.2

沈小平, 吴东, 于丽丽, 吴斌. 糖酵解-乳酸化修饰在哮喘中的潜在作用与治疗展望[J]. 中国临床药理学与治疗学, 2026, 31(1): 96-106.

Xiaoping SHEN, Dong WU, Lili YU, Bin WU. Potential role and therapeutic prospects of glycolysis-lactylation modification in asthma[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(1): 96-106.

图/表 3

图 1

Fig.1 Mechanism of glycolysis-lactate metabolism and lactylation in cells GLUT: glucose transporter; MCT: monocarboxylate transporter; LDH: lactate dehydrogenase; MGO: methylglyoxal; LGSH: S-D-lactoylglutathione; GLO1: glyoxalase 1; KAT: lysine acetyltransferase. This diagram was created using BioGDP.com.

图 2

Fig.2 Regulatory mechanism of glycolysis-lactation in immune cells This figure was created using the Created with BioGDP.com.

表 1

Table 1 Targeted therapeutics for glycolysis-lactylation

Target	Drug	References
LDHA	FX11, Oxalate, GSK2837808A	[81-83]
HK2	Bergenin, 3-BP, 2-Deoxy-D-glucose (2-DG)	[85,93]
PFKFB3	3PO	[86-87,94]
MCT	Phloretin, Quercetin, BAY-8002, 7ACC, AR-C155858, AZD3965, CHC, Syrosingopine	[87-88]
P300	A-485	[92]

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糖酵解-乳酸化修饰在哮喘中的潜在作用与治疗展望

Potential role and therapeutic prospects of glycolysis-lactylation modification in asthma

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