N6-methyladenosine modiﬁcation: A potential regulatory mechanism in spinal cord injury

Frontiers in Cellular Neuroscience, 2022 · DOI: 10.3389/fncel.2022.989637 · Published: September 23, 2022

Simple Explanation

N6-methyladenosine (m6A) modification, a common change in RNA after transcription, is important for how genes work in neurological diseases. Spinal cord injury (SCI) is a serious condition with a complex and not fully understood mechanism. Studies show m6A changes after SCI, affecting the spinal cord's environment. This review explores how m6A is dynamically regulated by 'writers,' 'erasers,' and 'readers.' It also looks at how m6A relates to changes in the spinal cord's environment after injury, including cell death, axon regeneration, and scar formation. This information could lead to new ways to help the spinal cord recover. The review summarizes current research on m6A modification, focusing on its regulatory role in nerve dysfunction and tissue repair after SCI. It aims to provide a basis for future research and clinical strategies to improve spinal cord function recovery.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review article

Key Findings

1
m6A modification levels change after spinal cord injury (SCI), and m6A-related regulators are involved in the changes of the local spinal cord microenvironment after injury.
2
Specific knockout of mettl14, a writer, helps functional recovery after SCI and reduces neuronal apoptosis, indicating that dynamic m6A modification has a strong potential to regulate the injury mechanism after SCI and influencing functional recovery.
3
m6A modification can regulate the physiological functions of astrocytes, and changes in m6A modification affect the aggregation of astrocytes following SCI, indicating that m6A modification is linked to astrocyte survival after SCI, which can alter scar formation.

Research Summary

This review discusses the current research on m6A modification and its relationship with pathophysiological processes after SCI, including cell death, axonal regeneration, and scarring. Research on the role of m6A modification in SCI is still in its infancy, with limited studies on the specific mechanism and regulatory molecules, highlighting the need for further research on the impact of demethylases and binding proteins after SCI. m6A modification could be a potential target for influencing the pathological process of SCI and promoting recovery of spinal cord function.

Practical Implications

Therapeutic Target Identification

m6A modification and its regulatory proteins ('writers', 'erasers', 'readers') could be potential therapeutic targets for SCI.

Functional Recovery Strategies

Modulating m6A levels could influence cell death, axonal regeneration, and scar formation, leading to strategies for improving functional recovery after SCI.

Further Mechanistic Research

Further research is needed to elucidate the specific mechanisms of m6A modification in SCI, especially regarding the roles of demethylases and binding proteins.

Study Limitations

1
Limited research on specific mechanisms of m6A modification after SCI.
2
Few studies on the impact of demethylases and binding proteins after SCI.
3
Research is limited to bioinformatics analysis of gene expression and differential expression at the tissue and cell levels.

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