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. 2019 Apr 10;10:382. doi: 10.3389/fphys.2019.00382

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Copyright © 2019 Thai, Seidlmayer, Miller, Ferrero, Dorn, Schaefer, Bers and Dedkova.

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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Mitophagy signaling pathway was upregulated in the aging heart but severely impaired in HF. (A) Expression of the proteins in PINK-Parkin mitophagy pathway in cardiac myocytes from young, aged and failing hearts: PINK-1, Parkin, mitofusin 2 (MFN2), dynamin-related protein 1 (DRP1), SQSTM1/p62, pro-LC3, and LC3-I/LC3-II. GAPDH staining was used to confirm equal protein loading for each experimental group. (B–H) Summary analysis of PINK-1, Parkin, mitofusin 2 (MFN2), DRP1, SQSTM1/p62, pro-LC3, LC3-I protein expression normalized to GAPDH or VDAC1 as indicated in the figure. (I) Quantification of LC3-I conversion to LC3-II protein expression presented as LC3-II/LC3-I ratio. Data expressed as mean ± SEM. n = 3–5 animals per group, *p < 0.05 reflects a difference in aging and HF hearts vs. young hearts, #p < 0.05 reflects a difference in HF hearts vs. corresponding age-matched control hearts.