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. 2018 May 3;9:453. doi: 10.3389/fphys.2018.00453

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Copyright © 2018 Toedebusch, Belenchia and Pulakat.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Evidence for and against the existence of diabetic cardiomyopathy. Venn diagrams show the current evidence for (Panel A, green) and against (Panel B, red) the existence of diabetic cardiomyopathy, and how they relate to T1DM, T2DM, and/or both. Molecular/physiological mechanisms documented in rodent models include oxidative stress, glucotoxicity, lipotoxicity, metabolic inflexibility, cardiac fibrosis, and mitochondrial dysfunction (Boudina et al., 2005; Schilling and Mann, 2014; Holscher et al., 2016). Diastolic dysfunction implies heart failure with either preserved (HFpEF) or reduced (HFrEF) ejection fraction. HF = heart failure, T1DM = type 2 diabetes, T2DM = type 2 diabetes, and LV = left ventricle. ^∗∗Indicates possible sex difference documented in literature.