The physiological and clinical importance of sodium potassium ATPase in cardiovascular diseases.

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  • Author(s): Yan Y;Yan Y; Shapiro JI; Shapiro JI
  • Source:
    Current opinion in pharmacology [Curr Opin Pharmacol] 2016 Apr; Vol. 27, pp. 43-9. Date of Electronic Publication: 2016 Feb 15.
  • Publication Type:
    Journal Article; Research Support, N.I.H., Extramural; Review
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Elsevier Science Ltd Country of Publication: England NLM ID: 100966133 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1471-4973 (Electronic) Linking ISSN: 14714892 NLM ISO Abbreviation: Curr Opin Pharmacol Subsets: MEDLINE
    • Publication Information:
      Original Publication: Oxford : Elsevier Science Ltd., 2001-
    • Subject Terms:
    • Abstract:
      The Na/K-ATPase has been extensively studied, but it is only recently that its role as a scaffolding and signaling protein has been identified. It has been identified that cardiotonic steroids (CTS) such as digitalis mediate signal transduction through the Na/K-ATPase in a process found to result in the generation of reactive oxygen species (ROS). As these ROS also appear capable of initiating this signal cascade, a feed forward amplification process has been postulated and subsequently implicated in some disease pathways including uremic cardiomyopathy.
      (Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.)
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    • Grant Information:
      U01 HL071556 United States HL NHLBI NIH HHS; HL105649 United States HL NHLBI NIH HHS; R01 HL109015 United States HL NHLBI NIH HHS; HL071556 United States HL NHLBI NIH HHS; R01 HL105649 United States HL NHLBI NIH HHS; HL109015 United States HL NHLBI NIH HHS
    • Accession Number:
      0 (Cardiac Glycosides)
      0 (Reactive Oxygen Species)
      EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
    • Publication Date:
      Date Created: 20160219 Date Completed: 20161213 Latest Revision: 20240610
    • Publication Date:
      20240610
    • Accession Number:
      PMC5161351
    • Accession Number:
      10.1016/j.coph.2016.01.009
    • Accession Number:
      26891193