O-GlcNAcylation: a pro-survival response to acute stress in the cardiovascular and central nervous systems.

Cardioprotection Hexosamine biosynthetic pathway Neuroprotection O-GlcNAcylation Stress tolerance

Journal

European journal of medical research
ISSN: 2047-783X
Titre abrégé: Eur J Med Res
Pays: England
ID NLM: 9517857

Informations de publication

Date de publication:
16 Mar 2024
Historique:
received: 19 08 2023
accepted: 06 03 2024
medline: 18 3 2024
pubmed: 16 3 2024
entrez: 16 3 2024
Statut: epublish

Résumé

O-GlcNAcylation is a unique monosaccharide modification that is ubiquitously present in numerous nucleoplasmic and mitochondrial proteins. The hexosamine biosynthesis pathway (HBP), which is a key branch of glycolysis, provides the unique sugar donor UDP-GlcNAc for the O-GlcNAc modification. Thus, HBP/O-GlcNAcylation can act as a nutrient sensor to perceive changes in nutrient levels and trigger O-GlcNAc modifications of functional proteins in cellular (patho-)physiology, thereby regulating diverse metabolic processes. An imbalance in O-GlcNAcylation has been shown to be a pathogenic contributor to dysfunction in metabolic diseases, including type 2 diabetes, cancer, and neurodegeneration. However, under acute stress conditions, protein O-GlcNAc modification exhibits rapid and transient upregulation, which is strongly correlated with stress tolerance and cell survival. In this context, we discuss the metabolic, pharmacological and genetic modulation of HBP/O-GlcNAc modification in the biological system, the beneficial role of O-GlcNAcylation in regulating stress tolerance for cardioprotection, and neuroprotection, which is a novel and rapidly growing field. Current evidence suggests that transient activation of the O-GlcNAc modification represents a potent pro-survival signalling pathway and may provide a promising strategy for stress-related disorder therapy.

Identifiants

pubmed: 38491477
doi: 10.1186/s40001-024-01773-z
pii: 10.1186/s40001-024-01773-z
pmc: PMC10943874
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

174

Subventions

Organisme : Priority Academic Program Development of Jiangsu Higher Education Institutions
ID : PAPD
Organisme : Municipal Health Commission of Nantong
ID : MSZ2022048
Organisme : National Natural Science Foundation of China
ID : 81401094

Informations de copyright

© 2024. The Author(s).

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Auteurs

Qiu Xue (Q)

Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, 19 Qixiu Road, Nantong, 226001, China.
Department of General Surgery, Nantong Tumor Hospital, Nantong Fifth People's Hospital, Affiliated Tumor Hospital of Nantong University, 30 Tongyang North Road, Nantong, 226361, China.

Shengtao Ji (S)

Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, 19 Qixiu Road, Nantong, 226001, China.
Department of Neurology, Affiliated Hospital of Nantong University, Medical School of Nantong University, 20 Xisi Road, Nantong, 226001, China.

Hui Xu (H)

Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, 19 Qixiu Road, Nantong, 226001, China.
Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity & Child Healthcare Hospital of Nantong University, 399 Century Avenue, Nantong, 226001, China.

Shu Yu (S)

Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, 19 Qixiu Road, Nantong, 226001, China. yushu@ntu.edu.cn.

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