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• W3035100413 abstract "Cardiac hypertrophy without appropriate treatment eventually progresses to heart failure. Our recent data demonstrated that the immunoproteasome subunit β5i promotes cardiac hypertrophy. However, whether β5i is a promising therapeutic target for treating hypertrophic remodeling remains unknown. Here we investigated the effects of PR-957, a β5i-specific inhibitor, on angiotensin II (Ang II)–induced hypertrophic remodeling in the murine heart. The infusion of Ang II increased immunoproteasome chymotrypsin-like activity and β5i catalytic subunit expression in the heart, whereas PR-957 treatment fully blocked the enhanced immunoproteasome activity caused by Ang II. Moreover, the administration of PR-957 significantly suppressed Ang II–induced cardiac hypertrophy, fibrosis, and inflammation. Mechanistically, PR-957 treatment inhibited phosphatase and tensin homologue on chromosome ten (PTEN) degradation, thereby inhibiting multiple signals including AKT/mTOR, ERK1/2, transforming growth factor-β, and IKB/NF-kB. Furthermore, PTEN blocking by its specific inhibitor VO-OHpic markedly attenuated the inhibitory effect of PR-957 on Ang II–induced cardiac hypertrophy in mice. We conclude that PR-957 blocks PTEN degradation and activates its downstream mediators, thereby attenuating Ang II–induced cardiac hypertrophy. These findings highlight that PR-957 may be a potential therapeutic agent for Ang II-induced hypertrophic remodeling." @default.
• W3035100413 created "2020-06-19" @default.
• W3035100413 creator A5015105154 @default.
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• W3035100413 date "2020-06-12" @default.
• W3035100413 modified "2023-10-17" @default.
• W3035100413 title "Selective Inhibition of the Immunoproteasome β5i Prevents PTEN Degradation and Attenuates Cardiac Hypertrophy" @default.
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• W3035100413 doi "https://doi.org/10.3389/fphar.2020.00885" @default.
• W3035100413 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7303343" @default.
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