Related Experiment Video
Updated: Jun 12, 2026
09:16
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
FoxO, autophagy, and cardiac remodeling
Anwarul Ferdous1, Pavan K Battiprolu, Yan G Ni
1Department of Internal Medicine (Division of Cardiology), University of Texas Southwestern Medical Center, NB11.200, 6000 Harry Hines Boulevard, Dallas, TX 75390-8573, USA.
Journal of Cardiovascular Translational Research
|June 26, 2010
Summary
The heart
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Biology
Background:
- The heart undergoes structural remodeling in response to workload changes.
- Physiological demand causes cardiac myocyte hypertrophy, while disease or unloading leads to adverse remodeling.
- FoxO transcription factors and autophagy are key regulators of cardiac growth and remodeling.
Purpose of the Study:
- To review recent advances in understanding cardiomyocyte autophagy.
- To explore the governance of autophagy by FoxO transcription factors.
- To elucidate the roles of autophagy and FoxO in cardiac remodeling.
Main Methods:
- Review of recent scientific literature on cardiac remodeling, FoxO, and autophagy.
- Discussion of molecular and cellular mechanisms.
- Synthesis of current understanding of FoxO-mediated regulation of autophagy in the heart.
Main Results:
- FoxO transcription factors are critical regulators of cell size, viability, and metabolism.
- Autophagy plays a pivotal role in cardiac growth and remodeling, with activated autophagy detected in myocardial disease.
- FoxO is an upstream regulator of both autophagy and the ubiquitin-proteasome system.
Conclusions:
- FoxO transcription factors are emerging as crucial regulators in the heart.
- Autophagy is a key pathway in cardiac remodeling and is regulated by FoxO.
- Understanding FoxO-mediated autophagy offers insights into cardiac disease and therapeutic strategies.
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