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.
|Number of pages||14|
|Journal||JACC: Basic to Translational Science|
|State||Published - Feb 2018|
Bibliographical noteFunding Information:
Dr. Manning has received grants from the American Heart Association (14POST20460224) and the NIH (F32HL126300). Dr. Withers has received an NIH grant (T32-HL0727423) and an NSF grant (DGE-1247392). Dr. Nagareddy has received an NIH grant (R00 HL22505). Dr. Abdel-Latif has received NIH grants (UK Cobre NIH P20 GM 103527 and NIH R56 HL124266). Drs. Withers and Andres has received the IDeA award 8 P20 GM103527. Drs. Andres and Satin have received grants from the NIH (R56HL131782) and the American Heart Association (GRNT27790094). Dr. Andres has received a UK Research Professorship. Dr. Satin has received an NIH grant (R01 HL074091). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
© 2018 The Authors
- calcium channel
- myocardial infarction
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine