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. 2020 Jan 23;10:1630. doi: 10.3389/fphys.2019.01630

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Copyright © 2020 Federico, Valverde, Mattiazzi and Palomeque.

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(s) 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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RyR2 dysregulation in DCM development. (A) Representative ECG recordings showing that fructose-rich diet (FRD) induces cardiac arrhythmias in WT but not in SR-AIP mice (CD, control diet). WT mice exhibit bradycardia (ii), bidirectional tachycardia (iii), ventricular ectopic beats (iv, arrow), and AV block (v, arrow) when treated with FRD. (B) FRD deteriorates mitochondria membrane potential, as shown by an increase in JC-1 green/red fluorescence ratio. (C) This alteration in FRD mitochondria is in accordance with a higher apoptotic ratio (Bax/Bcl-2 proteins), which can be prevented in mice expressing the CaMKII inhibitory peptide at the SR level (SR-AIP). (D) Histological samples (upper right) show a closer distance between mitochondria and SR in FRD vs. CD treated mice, which might be due to an alteration in structural proteins involved in SR-mitochondria communication. The cartoon in the left side of (D) represents this SR-mito interaction (reproduced with permission from Federico et al., 2017). *p < 0.05.