title: Hypoxia-dependent reactive oxygen species signaling in the pulmonary circulation: focus on ion channels.
abstract: CONCLUSIONS
  An acute lack of oxygen in the lung causes hypoxic pulmonary vasoconstriction, which optimizes gas exchange. In contrast, chronic hypoxia triggers a pathological vascular remodeling causing pulmonary hypertension, and ischemia can cause vascular damage culminating in lung edema.
  
  
  BACKGROUND
  Regulation of ion channel expression and gating by cellular redox state is a widely accepted mechanism; however, it remains a matter of debate whether an increase or a decrease in reactive oxygen species (ROS) occurs under hypoxic conditions. Ion channel redox regulation has been described in detail for some ion channels, such as Kv channels or TRPC6. However, in general, information on ion channel redox regulation remains scant.
  
  
  CONCLUSIONS
  In addition to the debate of increased versus decreased ROS production during hypoxia, we aim here at describing and deciphering why different oxidants, under different conditions, can cause both activation and inhibition of channel activity. While the upstream pathways affecting channel gating are often well described, we need a better understanding of redox protein modifications to be able to determine the complexity of ion channel redox regulation. Against this background, we summarize the current knowledge on hypoxia-induced ROS-mediated ion channel signaling in the pulmonary circulation.
authors.affiliation: 1 Excellence Cluster Cardiopulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), German Center for Lung Research (DZL) , Giessen, Germany .
authors.forename: Florian
authors.initials: F
authors.lastname: Veit
authors.forename: Oleg
authors.initials: O
authors.lastname: Pak
authors.forename: Ralf P
authors.initials: RP
authors.lastname: Brandes
authors.forename: Norbert
authors.initials: N
authors.lastname: Weissmann
mesh_terms: D000818:Animals; D015687:Cell Hypoxia; D006801:Humans; D007473:Ion Channels / Q000378:metabolism*; D010084:Oxidation-Reduction; D011188:Potassium / Q000378:metabolism*; D011652:Pulmonary Circulation; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction; D050052:TRPC Cation Channels / Q000378:metabolism; D000074287:TRPC6 Cation Channel
chemical_list: D007473:Ion Channels; D017382:Reactive Oxygen Species; D050052:TRPC Cation Channels; D000074287:TRPC6 Cation Channel; C117032:TRPC6 protein, human; D011188:Potassium