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Updated: Jul 19, 2026

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
Published on: July 14, 2021
Thioredoxin and ventricular remodeling
Tetsuro Ago1, Junichi Sadoshima
1Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, 185 South Orange Avenue, Medical Science Building G-609, Newark, NJ 07103, USA.
Abstract:
Increasing bodies of evidence indicate that reactive oxygen species (ROS) produced by mitochondria and other sources play an essential role in mediating ventricular remodeling after myocardial infarction and the development of heart failure. Antioxidants scavenge ROS, thereby maintaining the reduced environment of cells and inhibiting ventricular remodeling in the heart. Thioredoxin not only functions as a major antioxidant in the heart but also interacts with important signaling molecules and transcription factors, thereby modulating various cellular functions. The activity of thioredoxin is regulated by a variety of mechanisms, such as transcription, localization, protein-protein interaction, and post-translational modification. In this review, we will summarize the cardiac effects of thioredoxin and the mechanisms by which thioredoxin mediates inhibition of ventricular remodeling.
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