The role of N6-methyladenosine modification in rodent models of neuropathic pain: from the mechanism to therapeutic potential

Abstract

Neuropathic pain (NP) is a common chronic pain condition resulted from lesions or diseases of somatosensory nervous system, but the pathogenesis remains unclear. A growing body of evidence supports the relationship between pathogenesis and N6-methyladenosine (m6A) modifications of RNA. However, studies on the role of m6A modifications in NP are still at an early stage. Elucidating different etiologies is important for understanding the specific pathogenesis of NP. This article provides a comprehensive review on the role of m6A methylation modifications including methyltransferases (''writers''), demethylases (''erasers''), and m6A binding proteins (''readers'') in NP models. Further analysis of the pathogenic mechanism relationship between m6A and NP provided novel theoretical and practical significance for clinical treatment of NP.

Keywords

• M6A methylation modification
• Neuropathic pain
• Rodent model
• Mechanism of action
• Targeted therapy