Nociceptive Roles of TRPM2 Ion Channel in Pathologic Pain

被引:25
|
作者
Jang, Yongwoo [1 ,2 ]
Cho, Pyung Sun [3 ,4 ]
Yang, Young Duk [5 ]
Hwang, Sun Wook [3 ,4 ]
机构
[1] Harvard Med Sch, McLean Hosp, Dept Psychiat, Belmont, MA 02478 USA
[2] Harvard Med Sch, McLean Hosp, Program Neurosci, Belmont, MA 02478 USA
[3] Korea Univ, Coll Med, Dept Biomed Sci, Seoul 02841, South Korea
[4] Korea Univ, Coll Med, Dept Physiol, Seoul 02841, South Korea
[5] CHA Univ, Coll Pharm, Dept Pharm, Gyeonggi 11160, South Korea
基金
新加坡国家研究基金会;
关键词
TRPM2; Oxidative stress; Pain; Nociceptor; Immune cell; DORSAL-ROOT GANGLION; POTENTIAL MELASTATIN 2; SPINAL-CORD-INJURY; PERIPHERAL NERVOUS-SYSTEM; INDUCED OXIDATIVE STRESS; CYCLIC ADP-RIBOSE; PROTEIN-KINASE; CA2+ INFLUX; HYDROGEN-PEROXIDE; TRPV1; CHANNELS;
D O I
10.1007/s12035-017-0862-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Pain is a protective mechanism that enables us to avoid potentially harmful environments. However, when pathologically persisted and aggravated under severely injured or inflamed conditions, pain often reduces the quality of life and thus is considered as a disease to eliminate. Inflammatory and/or neuropathic mechanisms may exaggerate interactions between damaged tissues and neural pathways for pain mediation. Similar mechanisms also promote the communication among cellular participants in synapses at spinal or higher levels, which may amplify nociceptive firing and subsequent signal transmission, deteriorating the pain sensation. In this pathology, important cellular players are afferent sensory neurons, peripheral immune cells, and spinal glial cells. Arising from damage of injury, overloaded interstitial and intracellular reactive oxygen species (ROS) and intracellular Ca2+ are key messengers in the development and maintenance of pathologic pain. Thus, an ROS-sensitive and Ca2+-permeable ion channel that is highly expressed in the participant cells might play a critical role in the pathogenesis. Transient receptor potential melastatin subtype 2 (TRPM2) is the unique molecule that satisfies all of the requirements: the sensitivity, permeability, and its expressing cells. Notable progress in delineating the role of TRPM2 in pain has been achieved during the past decade. In the present review, we summarize the important findings in the key cellular components that are involved in pathologic pain. This overview will help to understand TRPM2-mediated pain mechanisms and speculate therapeutic strategies by utilizing this updated information.
引用
收藏
页码:6589 / 6600
页数:12
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