Abstract
Oxidative stress in cardiac disease promotes pro-arrhythmic disturbances in Ca2+ homeostasis. This includes impaired luminal Ca2+ regulation of the sarcoplasmic reticulum (SR) Ca2+ release channel the ryanodine receptor (RyR2), driving increased channel activity. However, exact mechanisms underlying the redox-mediated increase of RyR2 function in cardiac disease remain elusive. Using a rat model of hypertrophy induced by thoracic aorta banding (TAB), we tested whether oxidoreductase proteins that dynamically regulate the SR oxidative environment are involved in this process.
Full Text 
Sign-in/Register to access full text options
Sign-in/Register to access full text options 
Published version (
Free)
Free) 
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 call
