O-GlycNacylation Remission Retards the Progression of Non-Alcoholic Fatty Liver Disease

Yicheng Zhou; Zhangwang Li; Minxuan Xu; Deju Zhang; Jitao Ling; Peng Yu; Yunfeng Shen

doi:10.3390/cells11223637

O-GlycNacylation Remission Retards the Progression of Non-Alcoholic Fatty Liver Disease

Cells. 2022 Nov 16;11(22):3637. doi: 10.3390/cells11223637.

Authors

Yicheng Zhou¹, Zhangwang Li², Minxuan Xu¹, Deju Zhang³, Jitao Ling¹, Peng Yu¹, Yunfeng Shen¹

Affiliations

¹ Department of Endocrinology and Metabolism, the Second Affiliated Hospital of Nanchang University, Branch of Nationlal Clinical Research Center for Metabolic Diseases, Institute for the Study of Endocrinology and Metabolism in Jiangxi Province, Nanchang 330006, China.
² The Second Clinical Medical College of Nanchang University, Nanchang 330031, China.
³ Food and Nutritional Sciences, School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Hong Kong.

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a metabolic disease spectrum associated with insulin resistance (IR), from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). O-GlcNAcylation is a posttranslational modification, regulated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). Abnormal O-GlcNAcylation plays a key role in IR, fat deposition, inflammatory injury, fibrosis, and tumorigenesis. However, the specific mechanisms and clinical treatments of O-GlcNAcylation and NAFLD are yet to be elucidated. The modification contributes to understanding the pathogenesis and development of NAFLD, thus clarifying the protective effect of O-GlcNAcylation inhibition on liver injury. In this review, the crucial role of O-GlcNAcylation in NAFLD (from NAFL to HCC) is discussed, and the effect of therapeutics on O-GlcNAcylation and its potential mechanisms on NAFLD have been highlighted. These inferences present novel insights into the pathogenesis and treatments of NAFLD.

Keywords: O-GlcNAcylation; cirrhosis; fibrosis; hepatocellular carcinoma; insulin resistance; non-alcoholic fatty liver disease; non-alcoholic steatohepatitis.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Carcinoma, Hepatocellular* / complications
Humans
Insulin Resistance*
Liver Neoplasms* / complications
Non-alcoholic Fatty Liver Disease* / metabolism
Protein Processing, Post-Translational

Grants and funding

This work was supported by the National Natural Science Foundation of China [grant number No.82160170 and No.81860151]; the National Key R&D Program of China, Synthetic Biology Research [No.2019YFA0904500]; the Key R&D Program of Jiangxi Province [No. 20192BBG70027]; the National Clinical Research Center for Geriatrics—JiangXi branch center [No. 2021ZDG02001]; [No. 20212BAB216047 and No. 202004BCJL23049], and the National Natural Science Foundation of China [grant number No. 82100869].