REDD1 attenuates cardiac hypertrophy via enhancing autophagy

Chen Liu, Ruicong Xue, Dexi Wu, Lingling Wu, Cong Chen, Weiping Tan, Yili Chen, Yugang Dong

Research output: Contribution to journalArticlepeer-review

31 Scopus citations

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.

Original languageEnglish
Pages (from-to)215-220
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume454
Issue number1
DOIs
StatePublished - 7 Nov 2014
Externally publishedYes

Keywords

  • Autophagy
  • Cardiac hypertrophy
  • REDD1
  • mTOR

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