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Implications of SGLT inhibition on redox signalling in atrial fibrillation

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Item Type:Review
Title:Implications of SGLT inhibition on redox signalling in atrial fibrillation
Creators Name:Bode, D. and Semmler, L. and Oeing, C.U. and Alogna, A. and Schiattarella, G.G. and Pieske, B.M. and Heinzel, F.R. and Hohendanner, F.
Abstract:Atrial fibrillation (AF) is the most common sustained (atrial) arrhythmia, a considerable global health burden and often associated with heart failure. Perturbations of redox signalling in cardiomyocytes provide a cellular substrate for the manifestation and maintenance of atrial arrhythmias. Several clinical trials have shown that treatment with sodium-glucose linked transporter inhibitors (SGLTi) improves mortality and hospitalisation in heart failure patients independent of the presence of diabetes. Post hoc analysis of the DECLARE-TIMI 58 trial showed a 19% reduction in AF in patients with diabetes mellitus (hazard ratio, 0.81 (95% confidence interval: 0.68-0.95), n = 17.160) upon treatment with SGLTi, regardless of pre-existing AF or heart failure and independent from blood pressure or renal function. Accordingly, ongoing experimental work suggests that SGLTi not only positively impact heart failure but also counteract cellular ROS production in cardiomyocytes, thereby potentially altering atrial remodelling and reducing AF burden. In this article, we review recent studies investigating the effect of SGLTi on cellular processes closely interlinked with redox balance and their potential effects on the onset and progression of AF. Despite promising insight into SGLTi effect on Ca(2+) cycling, Na(+) balance, inflammatory and fibrotic signalling, mitochondrial function and energy balance and their potential effect on AF, the data are not yet conclusive and the importance of individual pathways for human AF remains to be established. Lastly, an overview of clinical studies investigating SGLTi in the context of AF is provided.
Keywords:Atrial Fibrillation, Heart Failure, SGLT Inhibition, Cardiomyocytes, Redox Signalling, Reactive Oxygen Species, Oxidative Stress, Mitochondrial Function, Ca(2+) Homeostasis, Animals
Source:International Journal of Molecular Sciences
Page Range:5937
Date:31 May 2021
Official Publication:https://doi.org/10.3390/ijms22115937
PubMed:View item in PubMed

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