Nociceptive Roles of TRPM2 Ion Channel in Pathologic Pain

Yongwoo Jang, Pyung Sun Cho, Young Duk Yang, Sun Wook Hwang

Research output: Contribution to journalReview articlepeer-review

22 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)6589-6600
Number of pages12
JournalMolecular Neurobiology
Issue number8
Publication statusPublished - 2018 Aug 1

Bibliographical note

Funding Information:
This work was supported by grants from the National Research Foundation of Korea (2017R1A2B2001817 and 2017M3C7A1025600).

Publisher Copyright:
© 2018, Springer Science+Business Media, LLC, part of Springer Nature.


  • Immune cell
  • Nociceptor
  • Oxidative stress
  • Pain
  • TRPM2

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience


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