Redox Regulation of Transient Receptor Potential Channels in the Endothelium

Authors

  • Paulo Wagner Pires,

    1. Department of Pharmacology, Cardiovascular Research Center, University of Nevada, Reno School of Medicine, Reno, NV, USA
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  • Scott Earley

    Corresponding author
    1. Department of Pharmacology, Cardiovascular Research Center, University of Nevada, Reno School of Medicine, Reno, NV, USA
    • Address for correspondence: Scott Earley, Ph.D.

      Department of Pharmacology/MS 0318

      University of Nevada, Reno School of Medicine

      Manville Health Sciences Building Room 8

      Reno, NV 89557-0318, USA

      Phone: (775) 784-4117

      Fax: (775) 784-1620

      Email: searley@medicine.nevada.edu

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  • This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/micc.12329

Abstract

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are important mediators of signaling pathways in the endothelium. Specific members of the transient receptor potential (TRP) superfamily of cation channels act as important Ca2+ influx pathways in endothelial cells, and are involved in endothelium-dependent vasodilation, regulation of barrier permeability, and angiogenesis. ROS and RNS can modulate the activity of certain TRP channels mainly by modifying specific cysteine residues or by stimulating the production of second messengers. In this review we highlight the recent literature describing in redox regulation of TRP channel activity in endothelial cells as well as the physiological importance of these pathways and implication for cardiovascular diseases.

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