title: Redox regulation of transient receptor potential channels.
abstract: CONCLUSIONS
  Environmental and endogenous reactive species such as reactive oxygen species (ROS), reactive nitrogen species (RNS), and other electrophiles are not only known to exert toxic effects on organisms, but are also emerging as molecules that mediate cell signaling responses. However, the mechanisms underlying this cellular redox signaling by reactive species remains largely uncharacterized.
  
  
  BACKGROUND
  Ca2+-permeable cation channels encoded by the transient receptor potential (trp) gene superfamily are characterized by a wide variety of activation triggers that act from outside and inside the cell. Recent studies have revealed that multiple TRP channels sense reactive species and induce diverse physiological and pathological responses, such as cell death, chemokine production, and pain transduction. TRP channels sense reactive species either indirectly through second messengers or directly via oxidative modification of cysteine residues. In this review, we describe the activation mechanisms and biological roles of redox-sensitive TRP channels, including TRPM2, TRPM7, TRPC5, TRPV1, and TRPA1.
  
  
  RESULTS
  The sensitivity of TRP channels to reactive species in vitro has been well characterized using molecular and pharmacological approaches. However, the precise activation mechanism(s) and in vivo function(s) of ROS/RNS-sensitive TRP channels remain elusive.
  
  
  CONCLUSIONS
  Redox sensitivity of TRP channels has been shown to mediate previously unexplained biological phenomena and is involved in various pathologies. Understanding the physiological significance and activation mechanisms of TRP channel regulation by reactive species may lead to TRP channels becoming viable pharmacological targets, and modulators of these channels may offer therapeutic options for previously untreatable diseases.
authors.affiliation: 1 Department of Synthetic Chemistry and Biological Chemistry, Graduate School of Engineering, Kyoto University , Kyoto, Japan .
authors.forename: Daisuke
authors.initials: D
authors.lastname: Kozai
authors.forename: Nozomi
authors.initials: N
authors.lastname: Ogawa
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Mori
mesh_terms: D000818:Animals; D006801:Humans; D010084:Oxidation-Reduction; D026361:Reactive Nitrogen Species / Q000378:metabolism; D050052:TRPC Cation Channels / Q000378:metabolism; D050053:TRPM Cation Channels / Q000378:metabolism; D050916:TRPV Cation Channels / Q000378:metabolism; D050051:Transient Receptor Potential Channels / Q000378:metabolism*
chemical_list: D026361:Reactive Nitrogen Species; D050052:TRPC Cation Channels; D050053:TRPM Cation Channels; D050916:TRPV Cation Channels; D050051:Transient Receptor Potential Channels