Related Experiment Video
Updated: Apr 20, 2026
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
REDD1 attenuates cardiac hypertrophy via enhancing autophagy
Chen Liu1, Ruicong Xue1, Dexi Wu1
1Department of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, China; Key Laboratory on Assisted Circulation, Ministry of Health, Guangzhou 510080, China.
Insights
REDD1 protein is crucial for preventing cardiac hypertrophy by enhancing autophagy. Its deficiency worsens heart enlargement and impairs autophagy, highlighting REDD1
Area of Science:
- Cardiovascular Biology
- Cellular Stress Response
- Molecular Cardiology
Background:
- Cardiac hypertrophy is a significant risk factor for cardiovascular disease.
- Autophagy plays a key role in regulating cardiac hypertrophy.
- REDD1 is a stress-responsive protein involved in autophagy induction, but its role in cardiac hypertrophy is unclear.
Purpose of the Study:
- To investigate the role of REDD1 in phenylephrine (PE)-induced cardiac hypertrophy.
- To elucidate the underlying mechanisms, including autophagy and ERK1/2 signaling.
Main Methods:
- RNA interference (RNAi) to knockdown REDD1 in cardiomyocytes.
- Assessment of hypertrophic markers (e.g., ANP, cell surface area).
- Analysis of autophagy flux, ERK1/2 signaling, and mTOR pathway activation.
Main Results:
- REDD1 knockdown exacerbated PE-induced cardiac hypertrophy and increased hypertrophic markers.
- REDD1 deficiency impaired autophagy and activated mTOR signaling under PE stress.
- ERK1/2 signaling was implicated in REDD1's effect on hypertrophy.
- Rapamycin treatment reversed the pro-hypertrophic effects of REDD1 knockdown.
Conclusions:
- REDD1 is essential for inhibiting cardiac hypertrophy.
- REDD1 promotes autophagy, thereby protecting against cardiac hypertrophy.
- Targeting REDD1-mediated autophagy may offer a therapeutic strategy for cardiac hypertrophy.
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.
Related Concept Videos
01:26Cellular Adaptation II: Hypertrophy
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:29Heart Failure II: Pathophysiology
01:27Autophagy
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...