REDD1 attenuates cardiac hypertrophy via enhancing autophagy |
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Authors: | Chen Liu Ruicong Xue Dexi Wu Lingling Wu Cong Chen Weiping Tan Yili Chen Yugang Dong |
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Affiliation: | 1. Department of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, China;2. Key Laboratory on Assisted Circulation, Ministry of Health, Guangzhou 510080, China;3. Department of Respiratory, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, China |
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Abstract: | Cardiac hypertrophy is a major risk factor of cardiovascular morbidity and mortality. Autophagy is established to be involved in regulating cardiac hypertrophy. REDD1, a stress-responsive protein, is proved to contribute in autophagy induction. However, the role of REDD1 in cardiac hypertrophy remains unknown. Our study demonstrated that REDD1 knockdown by RNAi exacerbated phenylephrine (PE)-induced cardiac hypertrophy, manifested by increased hypertrophic markers such as ANP and cell surface area. In addition, we discovered that ERK1/2 signaling pathway was involved in the effect of REDD1 on hypertrophy. Moreover, our study showed that REDD1 knockdown impaired autophagy in hypertrophied cardiomyocytes. mTOR, a signaling molecule governing autophagy induction, was activated by the knockdown of REDD1 under PE stress. Importantly, the pro-hypertrophic effect of REDD1 knockdown was significantly reversed by the autophagy enhancer rapamycin. Taken together, we firstly prove that REDD1 is essential for inhibiting cardiac hypertrophy by enhancing autophagy. |
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