Role of O-linked β-N-acetylglucosamine modification in metabolic associated fatty liver disease

Sutong LIU; Lihui ZHANG; Qing ZHAO; Weichen MA; Wanyi ZHU; Minghao LIU; Wenxia ZHAO

doi:10.12449/JCH260623

Volume 42 Issue 6

Jun. 2026

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Article Navigation > Journal of Clinical Hepatology > 2026 > 42(6): 1391-1397

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Role of O-linked β-N-acetylglucosamine modification in metabolic associated fatty liver disease

DOI: 10.12449/JCH260623

Sutong LIU^{1, 2
,
,
,},
Lihui ZHANG^{1, 2},
Qing ZHAO^{1, 2},
Weichen MA¹,
Wanyi ZHU¹,
Minghao LIU^{1, 2},
Wenxia ZHAO^{1, 2}

1.
Regional Diagnosis and Treatment Center for Hepatology，The First Affiliated Hospital of Henan University of Chinese Medicine，Zhengzhou 450000，China
2.
Collaborative Innovation Center of Prevention and Treatment of Major Diseases by Chinese and Western Medicine in Henan Province，Henan University of Chinese Medicine，Zhengzhou 450046，China

Research funding:

National Natural Science Foundation of China (82205086);

Specialized Standards for Henan Provincial Traditional Chinese Medicine Scientific Research Projects (2022JDZX114);

Young Elite Scientists Sponsorship Program by CAST (2023QNRC001);

Henan Province Traditional Chinese Medicine “Double First-Class” to Create a Scientific Research Project (HSRP-DFCTCM-2023-5-13);

Henan Province Postdoctoral Fund (HN2024080)

More Information

Corresponding author: LIU Sutong， qingteng1026@126.com （ORCID： 0000-0002-9124-1111）
Received Date: 2025-10-27
Accepted Date: 2025-12-15
Published Date: 2026-06-25

Abstract

Abstract

Metabolic associated fatty liver disease （MAFLD） is a chronic liver disease with a rapidly increasing incidence rate worldwide， and its complex pathogenesis is closely associated with O-linked β-N-acetylglucosamine （O-GlcNAc） modification. As a dynamic and reversible post-translational modification of proteins， O-GlcNAc modification is mainly regulated by O-GlcNAc transferase and O-GlcNAcase. O-GlcNAc modification can drive hepatic steatosis， exacerbate insulin resistance， and impair mitochondrial function， thereby leading to the aggravation of metabolic disorders， promoting inflammation response， and driving the progression of MAFLD to metabolic associated steatohepatitis and hepatic fibrosis. This article systematically reviews the latest research advances in the role of O-GlcNAc modification in the development and progression of MAFLD， in order to provide theoretical support and research direction for a deeper understanding of the pathological mechanism of MAFLD and the development of effective therapeutic strategies.
- Metabolic Associated Fatty Liver Disease,
- O-linked β-N-Acetylglucosamine,
- Protein Processing， Post-Translational

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References(38)

References

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Role of O-linked β-N-acetylglucosamine modification in metabolic associated fatty liver disease

DOI: 10.12449/JCH260623

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Role of O-linked β-N-acetylglucosamine modification in metabolic associated fatty liver disease

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