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

Liping Wu; Hongliang Tang

doi:10.1016/j.biopha.2023.115398

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

Biomed Pharmacother. 2023 Oct:166:115398. doi: 10.1016/j.biopha.2023.115398. Epub 2023 Aug 28.

Authors

Liping Wu¹, Hongliang Tang²

Affiliations

¹ Guangxi University of Traditional Chinese Medicine, Nanning, China; The First Clinical Medical College of Guangxi University of Traditional Chinese Medicine, Nanning, China.
² Guangxi Traditional Chinese Medicine University Affiliated Fangchenggang Hospital. Electronic address: tanghl2004@gxtcmu.edu.cn.

PMID: 37647691
DOI: 10.1016/j.biopha.2023.115398

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; Mechanism of action; Neuropathic pain; Rodent model; Targeted therapy.

Publication types

Review

MeSH terms

Adenosine
Animals
Chronic Pain*
Neuralgia* / drug therapy
Rodentia

Substances

Adenosine