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. 2021 Mar 18;12:634365. doi: 10.3389/fphar.2021.634365

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Copyright © 2021 Li, Meng, Han, Yang, Wang, Zhu, Cui, Zuo, Xu and Chang.

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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Vild prevents DCM and autophagy by regulating the miR-21/SPRY1/ERK/mTOR pathway. (A) M-mode echocardiograms and pulse-wave Doppler echocardiograms were used to examine cardiac function. Quantitative analysis of E/A (B), LVEF (C), LVFS (D), LVIDs (E), and LVIDd (F). Data are presented as mean ± SD. (G) Representative WB images of P62 and LC3. (H) Quantification P62 and LC3 protein levels. (I) Representative WB images of SPRY1, p-ERK, ERK, p-mTOR, and mTOR of cardiac tissues. (J) Quantification of SPRY1, p-ERK, ERK, p-mTOR, and mTOR protein levels. *p < 0.05. DM + AAV9 NC + vild, diabetic mice with no-load AAV9 and vild; DM + AAV9 + Vild, diabetic mice with AAV9-miR-21 and vild.