Trends in Cardiovascular Medicine
Volume 18, Issue 7 , Pages 233-239, October 2008

Cardioprotective Signaling by Endothelin☆

  • Anita Schorlemmer

      Affiliations

    • Center of Cardiovascular Research, Department of Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA
    • Department of Molecular Sciences and Bioengineering, University of Hawaii, Honolulu, HI 96822, USA
    • ,
  • Michelle L. Matter

      Affiliations

    • Department of Cell and Molecular Biology, University of Hawaii, Honolulu, HI 96813, USA
    • ,
  • Ralph V. Shohet

      Affiliations

    • Center of Cardiovascular Research, Department of Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA
    • Corresponding Author InformationAddress correspondence to: Dr. Ralph V. Shohet, Department of Medicine, University of Hawaii, Honolulu, HI 96813, USA. Tel.: (+1) 808 692 1469

The endothelin axis promotes vasoconstriction, suggesting that antagonists of endothelin signaling might be useful in treatment of heart failure. However, promising results from animal trials have not been recapitulated in heart failure patients. Here we review the role of major signaling pathways in the heart that are involved in cell survival initiated by ET-1. These pathways include mitogen-activated protein kinase, phosphatidyl inositol-1,4,5-triphosphate kinase (PI3K-AKT), nuclear factor-κB (NF-κB), and calcineurin signaling. A better understanding of endothelin-mediated signaling in cardiac cell survival may allow a reevaluation of endothelin receptor antagonists (ETRAs) in the treatment of heart failure.

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☆ This work was supported in part by grants from the NIH/NHLBI (HL64041 and HL073449) to RVS.

PII: S1050-1738(08)00128-X

doi:10.1016/j.tcm.2008.11.005

Trends in Cardiovascular Medicine
Volume 18, Issue 7 , Pages 233-239, October 2008

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