Antioxidant therapy for atrial fibrillation: lost in translation?

AF causes leak of Ca2+ from sarcoplasmic reticulum (SR), and decreases peak Na+ current and sarcoplasmic/endoplasmic reticulum calcium uptake (SERCA)-mediated SR Ca2+ uptake. 2 In addition, ROS can decrease connexin43 and impairs gap junction function probably via activation of c-Src tyrosine kinase. 7 In summary, there are a constellation of ion abnormalities, including abnormal intracellular Ca2+ handling, reduced repolarisation reserves, decreased peak sodium current, and weakened cardiomyocyte coupling. [...]ROS increases cardiac fibrosis by enhancing fibroblast proliferation and type I collagen gene expression, 8 and fibrosis is a known cause of AF. [...]oxidative stress refers to an imbalance between production and neutralisation, resulting in an excess amount of ROS, and activating natural antioxidant defence mechanisms of the cell is another potential therapeutic approach which could be exploited.