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Pharmaceuticals 2016, 9(3), 57; doi:10.3390/ph9030057

Targeting TRPM2 in ROS-Coupled Diseases

Division of Pharmacology, Faculty of Pharmaceutical Sciences, Teikyo Heisei University, Tokyo 164-8530, Japan
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Academic Editors: Arpad Szallasi and Susan M. Huang
Received: 23 May 2016 / Revised: 5 August 2016 / Accepted: 5 September 2016 / Published: 7 September 2016
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Abstract

Under pathological conditions such as inflammation and ischemia-reperfusion injury large amounts of reactive oxygen species (ROS) are generated which, in return, contribute to the development and exacerbation of disease. The second member of the transient receptor potential (TRP) melastatin subfamily, TRPM2, is a Ca2+-permeable non-selective cation channel, activated by ROS in an ADP-ribose mediated fashion. In other words, TRPM2 functions as a transducer that converts oxidative stress into Ca2+ signaling. There is good evidence that TRPM2 plays an important role in ROS-coupled diseases. For example, in monocytes the influx of Ca2+ through TRPM2 activated by ROS contributes to the aggravation of inflammation via chemokine production. In this review, the focus is on TRPM2 as a molecular linker between ROS and Ca2+ signaling in ROS-coupled diseases. View Full-Text
Keywords: TRPM2; Ca2+ signaling; reactive oxygen species; ROS-coupled diseases TRPM2; Ca2+ signaling; reactive oxygen species; ROS-coupled diseases
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Yamamoto, S.; Shimizu, S. Targeting TRPM2 in ROS-Coupled Diseases. Pharmaceuticals 2016, 9, 57.

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