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. 2018 Oct 5;8:14872. doi: 10.1038/s41598-018-33293-2

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic representation of the proposed mechanisms underlying diabetic cardiomyopathy in relation to sodium-glucose co-transporter (SGLT). Upregulation of SGLT in cardiomyocytes in the presence of diabetes mellitus results in an increase in sodium influx into cardiomyocytes that in turn increases cytosolic calcium loading via the sodium-calcium exchanger (NCX). Intracellular calcium overload can lead to (1) delayed after depolarizations (DADs), triggers for tachycardia, (2) impaired excitation-contraction coupling, and (3) activation of calcium-sensitive signaling pathways, leading to pathological changes.