DNA Methylation: A Target in Neuropathic Pain

被引：11
作者：
Jiang, Wei [1 ,2 ]
Tan, Xuan-Yu [3 ]
Li, Jia-Ming [4 ]
Yu, Peng [5 ]
Dong, Ming [1 ,2 ]
机构：
[1] First Hosp Jilin Univ, Dept Neurol, Changchun, Peoples R China
[2] First Hosp Jilin Univ, Neurosci Ctr, Changchun, Peoples R China
[3] First Hosp Jilin Univ, Dept Neurosurg, Changchun, Peoples R China
[4] First Hosp Jilin Univ, Dept Emergency, Changchun, Peoples R China
[5] Second Hosp Jilin Univ, Dept Ophthalmol, Changchun, Peoples R China
来源：
FRONTIERS IN MEDICINE | 2022年 / 9卷
基金：
中国国家自然科学基金;
关键词：
neuropathic pain; DNA methylation; gene suppression; epigenetic; treatment; DORSAL-ROOT GANGLION; CPG-BINDING PROTEIN-2; MAMMALIAN DNA; METHYLTRANSFERASE INHIBITORS; OPIOID RECEPTOR; DOWN-REGULATION; SEX-DIFFERENCES; TET PROTEINS; EXPRESSION; EPIGENETICS;
D O I：
10.3389/fmed.2022.879902
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Neuropathic pain (NP), caused by an injury or a disease affecting the somatosensory nervous system of the central and peripheral nervous systems, has become a global health concern. Recent studies have demonstrated that epigenetic mechanisms are among those that underlie NP; thus, elucidating the molecular mechanism of DNA methylation is crucial to discovering new therapeutic methods for NP. In this review, we first briefly discuss DNA methylation, demethylation, and the associated key enzymes, such as methylases and demethylases. We then discuss the relationship between NP and DNA methylation, focusing on DNA methyltransferases including methyl-CpG-binding domain (MBD) family proteins and ten-eleven translocation (TET) enzymes. Based on experimental results of neuralgia in animal models, the mechanism of DNA methylation-related neuralgia is summarized, and useful targets for early drug intervention in NP are discussed.
引用
收藏
页数：10
相关论文
共 103 条
[61]   Role of dorsal root ganglion K2P I.I in peripheral nerve injury-induced neuropathic pain [J].
Mao, Qingxiang ;
Yuan, Jingjing ;
Xiong, Ming ;
Wu, Shaogen ;
Chen, Liyong ;
Bekker, Alex ;
Tao, Yuan-Xiang ;
Yang, Tiande .
MOLECULAR PAIN, 2017, 13
[62]   HDAC inhibitors restore C-fibre sensitivity in experimental neuropathic pain model [J].
Matsushita, Yosuke ;
Araki, Kohei ;
Omotuyi, Olaposi Idowu ;
Mukae, Takehiro ;
Ueda, Hiroshi .
BRITISH JOURNAL OF PHARMACOLOGY, 2013, 170 (05) :991-998
[63]   BDNF as a pain modulator [J].
Merighi, Adalberto ;
Salio, Chiara ;
Ghirri, Alessia ;
Lossi, Laura ;
Ferrini, Francesco ;
Betelli, Chiara ;
Bardoni, Rita .
PROGRESS IN NEUROBIOLOGY, 2008, 85 (03) :297-317
[64]   MBD1 Contributes to the Genesis of Acute Pain and Neuropathic Pain by Epigenetic Silencing of Oprm1 and Kcna2 Genes in Primary Sensory Neurons [J].
Mo, Kai ;
Wu, Shaogen ;
Gu, Xiyao ;
Xiong, Ming ;
Cai, Weihua ;
Atianjoh, Fidelis E. ;
Jobe, Emily E. ;
Zhao, Xinyu ;
Tu, Wei-Feng ;
Tao, Yuan-Xiang .
JOURNAL OF NEUROSCIENCE, 2018, 38 (46) :9883-9899
[65]   DNA Methylation and Its Basic Function [J].
Moore, Lisa D. ;
Le, Thuc ;
Fan, Guoping .
NEUROPSYCHOPHARMACOLOGY, 2013, 38 (01) :23-38
[66]   Recruitment of DNA methyltransferase I to DNA repair sites [J].
Mortusewicz, O ;
Schermelleh, L ;
Walter, J ;
Cardoso, MC ;
Leonhardt, H .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (25) :8905-8909
[67]   Drugging the pain epigenome [J].
Niederberger, Ellen ;
Resch, Eduard ;
Parnham, Michael J. ;
Geisslinger, Gerd .
NATURE REVIEWS NEUROLOGY, 2017, 13 (07) :434-447
[68]   Brain feminization requires active repression of masculinization via DNA methylation [J].
Nugent, Bridget M. ;
Wright, Christopher L. ;
Shetty, Amol C. ;
Hodes, Georgia E. ;
Lenz, Kathryn M. ;
Mahurkar, Anup ;
Russo, Scott J. ;
Devine, Scott E. ;
McCarthy, Margaret M. .
NATURE NEUROSCIENCE, 2015, 18 (05) :690-+
[69]   CTCF is a uniquely versatile transcription regulator linked to epigenetics and disease [J].
Ohlsson, R ;
Renkawitz, R ;
Lobanenkov, V .
TRENDS IN GENETICS, 2001, 17 (09) :520-527
[70]   The colorful history of active DNA demethylation [J].
Ooi, Steen K. T. ;
Bestor, Timothy H. .
CELL, 2008, 133 (07) :1145-1148
234567891011