Rad GTPase Deletion Attenuates Post-Ischemic Cardiac Dysfunction and Remodeling

Janet R. Manning, Lakshman Chelvarajan, Bryana M. Levitan, Catherine N. Withers, Prabhakara R. Nagareddy, Christopher M. Haggerty, Brandon K. Fornwalt, Erhe Gao, Himi Tripathi, Ahmed Abdel-Latif, Douglas A. Andres, Jonathan Satin

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

The protein Rad interacts with the L-type calcium channel complex to modulate trigger Ca2+ and hence to govern contractility. Reducing Rad levels increases cardiac output. Ablation of Rad also attenuated the inflammatory response following acute myocardial infarction. Future studies to target deletion of Rad in the heart could be conducted to establish a novel treatment paradigm whereby pathologically stressed hearts would be given safe, stable positive inotropic support without arrhythmias and without pathological structural remodeling. Future investigations will also focus on establishing inhibitors of Rad and testing the efficacy of Rad deletion in cardioprotection relative to the time of onset of acute myocardial infarction.

Original languageEnglish
Pages (from-to)83-96
Number of pages14
JournalJACC: Basic to Translational Science
Volume3
Issue number1
DOIs
StatePublished - Feb 2018

Bibliographical note

Publisher Copyright:
© 2018 The Authors

Keywords

  • calcium channel
  • cardioprotection
  • inflammation
  • myocardial infarction

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint

Dive into the research topics of 'Rad GTPase Deletion Attenuates Post-Ischemic Cardiac Dysfunction and Remodeling'. Together they form a unique fingerprint.

Cite this