Mani Sadredini, Ravinea Manotheepan, Stephan E. Lehnart, Mark E. Anderson, Ivar Sjaastad and Mathis Korseberg Stokke
Oxidation of molecules in cardiac cells contributes to the development of arrhythmias, but oral antioxidants have failed to protect against arrhythmias in clinical trials. Targeted prevention of oxidation at specific molecular sites may be more efficient. Protection from oxidation of the cardiac enzyme calcium/calmodulin-dependent protein kinase II (CaMKII) has been suggested as an antiarrhythmic strategy. In a follow-up of a previous publication (Manotheepan et al. 2016, PMID: 27161030) PhD student Mani Sadredini and the Stokke group collaborated with Professor Stephan Lehnart from the University of Göttingen (Germany) and Professor Mark E. Anderson from the Johns Hopkins University, to combine mice with the inherited arrhythmia syndrome catecholaminergic polymorphic ventricular tachycardia (CPVT) with mice genetically protected against oxidation of CaMKII. While global reduction of oxidative stress from the strong antioxidant N-acetyl cysteine reduced arrhythmia-associated behavior in CPVT cells, specific protection against CaMKII did not. Other oxidation sensitive targets should be investigated to understand the role of oxidation in arrhythmias and the antiarrhythmic potential of antioxidants.
Read the article in Physiological Reports
doi: 10.14814/phy2.15030
