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Review | Open Access

O-linked β-N-acetylglucosamine modification in diabetic foot ulcer pathogenesis

Bingxue Qi1,‡, Siyang Chai2,‡, Yang Chen2, Guannan Zhou3, Peihong Li2, Xueqing Li2, Xiaodan Lu1( ), Li-Hao Huang4 ( )
Precision Molecular Medicine Center, Jilin Province People’s Hospital, 1183 Gongnong Road, Chaoyang District, Changchun 130021, China
Clinical Medicine College, Changchun University of Chinese Medicine, 1035 Boshuo Road, Jingyue District, Changchun 130117, China
Department of Gynecology, The Obstetrics and Gynecology Hospital of Fudan University, 419 Fang-Xie Road, Huangpu District, Shanghai 200011, China
Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Liver Cancer Institute, Zhongshan Hospital, Fudan University, 2005 Songhu,Yangpu District, Shanghai 200438, China

‡Bingxue Qi and Siyang Chai co-first authors.

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Highlights

• Elevated O-linked β-D-N-acetylglucosamine (O-GlcNAc) modification under high-glucose conditions contributes to diabetic foot ulcers (DFUs) pathogenesis by altering specific proteins involved in peripheral neuropathy, peripheral vascular disease, and chronic impaired wound healing.

• O-GlcNAc modification impacts distinct phases of the DFU healing process, including inflammation, granulation, and re-epithelialization.

• O-GlcNAc modification presents potential molecular targets for developing novel treatments for DFUs.

Abstract

O-linked β-D-N-acetylglucosamine (O-GlcNAc) modification represents a common form of posttranslational glycosylation orchestrated by two pivotal enzymes, namely, O-GlcNAc transferase and O-GlcNAcase. In recent years, emerging research has revealed a significant association between O-GlcNAc modification and the pathogenesis of diabetic foot ulcers (DFUs). Elevated O-GlcNAc levels under high-glucose conditions contribute to the pathogenesis of DFUs by modifying specific proteins, which are implicated in peripheral neuropathy, peripheral vascular disease, and impaired chronic wound healing. This process includes prolonged inflammation, compromised granulation tissue formation, disordered re-epithelialization, and blocked tissue remodelling. This review focuses on the pathogenesis of DFUs and on the correlation between protein O-GlcNAc modification and DFUs, offering potential new insights for the diagnosis and treatment of this condition.

Graphical Abstract

Keywords

O-linked β-D-N-acetylglucosamine modificationDiabetic foot ulcersPathogenesisperipheral neuropathyPeripheral arterial diseaseWound healingMetabolic dysregulationtherapeutic target

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Burns & Trauma
Volume 13 Issue 10,
October 2025
Article number: tkaf044
DOI: 10.1093/burnst/tkaf044

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Cite this article:
Qi B, Chai S, Chen Y, et al. O-linked β-N-acetylglucosamine modification in diabetic foot ulcer pathogenesis. Burns & Trauma, 2025, 13(10): tkaf044. https://doi.org/10.1093/burnst/tkaf044

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Received: 21 November 2024
Revised: 15 March 2025
Accepted: 11 July 2025
Published: 14 July 2025
© The Author(s) 2025. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.