Abstract
Overexpression of S100A6 from the S100 family of EF-hand Ca2+-binding proteins, decreases cardiomyocyte apoptosis in vitro, and as such is a potential therapeutic target for the prevention of adverse left ventricular (LV) remodeling following ischemia/reperfusion. Our recent data shows that S100A6 gene delivery attenuates LV systolic dysfunction after I/R. The purpose of our present study was to examine the effects of S100A6 on cardiomyocytes in vitro, examining apoptosis and regulation of calcium cycling at the level of sarcoplasmic reticulum, as well as to determine potential miRNAs involved in transcriptional and post-transcriptional regulation of S100A6 expression.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
