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. 2020 Jun 12;11:885. doi: 10.3389/fphar.2020.00885

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Copyright © 2020 Xie, Wang, Li, Deng, Bi, Zhang, Xia and Li

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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Working model of PR-957–mediated cardioprotection against Ang II–induced cardiac hypertrophy. Ang II upregulates β5i protein level and its corresponding chymotrypsin-like activity, which in turn promotes degradation of phosphatase and tensin homolog on chromosome ten (PTEN), leading to the activation of AKT/mTOR, TGF-β/Smad2/3, and p-IkBα/NF-KB, thereby resulting in cardiac hypertrophy, fibrosis, and inflammation. Conversely, the inhibition of β5i by PR-957 markedly reverses these effects. Casein Kinase II (CK2); Phosphoinositide 3-kinase (PI3K); protein kinase A (PKA); AMP-responsive element binding protein (CREB); myocyte enhancer factor 2 (MEF2).