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O-GlcNAc cycling in neuroinflammation: From molecular mechanisms and therapeutic perspectives
Chanhaeng Lee1, Sang-Min Kim1, Dong Yeol Kim1
1Department of Physiology and Biophysics, College of Medicine, Inha University, Incheon, Republic of Korea; Department of Biomedical Science, Program in Biomedical Science and Engineering, Inha University, Incheon, Republic of Korea.
Abstract:
O-GlcNAcylation is a dynamic post-translational modification that regulates diverse cellular processes by modifying nuclear and cytoplasmic proteins in response to metabolic cues. This modification is controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), which together maintain O-GlcNAc cycling. Emerging evidence indicates that O-GlcNAcylation plays a critical role in modulating neuroinflammation, a key pathological feature of many neurological disorders, including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. O-GlcNAcylation modulates several components of the neuroinflammatory cascade, including glial activation, cytokine production, oxidative stress, and inflammasome assembly, primarily through its influence on transcription factors such as NF-κB and STATs, as well as key signaling pathways like MAPK. In this review, we critically evaluate current insights into the mechanisms by which O-GlcNAc cycling regulates neuroinflammatory processes and discuss recent advances in therapeutic strategies targeting O-GlcNAc metabolism. These insights underscore the potential of modulating O-GlcNAcylation as a novel strategy for controlling neuroinflammation across a range of disease contexts.
Insights
O-GlcNAcylation, a cellular process regulated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), is crucial for controlling neuroinflammation. Modulating this process offers a promising therapeutic strategy for neurological disorders.
Area of Science:
- Biochemistry
- Neuroscience
- Cellular Biology
Background:
- O-GlcNAcylation is a dynamic post-translational modification regulating cellular functions.
- It is controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), maintaining O-GlcNAc cycling.
- Neuroinflammation is implicated in various neurological disorders like Alzheimer's, Parkinson's, and multiple sclerosis.
Purpose of the Study:
- To review the mechanisms by which O-GlcNAc cycling influences neuroinflammation.
- To discuss therapeutic strategies targeting O-GlcNAc metabolism for neurological diseases.
Main Methods:
- Literature review and critical evaluation of current research.
- Analysis of O-GlcNAcylation's role in neuroinflammatory pathways.
- Assessment of therapeutic potential of targeting O-GlcNAc metabolism.
Main Results:
- O-GlcNAcylation modulates glial activation, cytokine production, oxidative stress, and inflammasome assembly.
- It influences transcription factors (NF-κB, STATs) and signaling pathways (MAPK).
- Dysregulation of O-GlcNAc cycling is linked to neuroinflammatory pathogenesis.
Conclusions:
- O-GlcNAcylation is a key regulator of neuroinflammatory processes.
- Targeting O-GlcNAc metabolism presents a novel therapeutic avenue for neurological disorders.
- Further research into O-GlcNAc cycling could yield effective treatments for neuroinflammation.
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