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J Mol Cell Cardiol. 2006 Nov;41(5):762-73. Epub 2006 Sep 26.

Thioredoxin and ventricular remodeling.

Author information

1
Cardiovascular 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.

PMID:
17007870
PMCID:
PMC1852508
DOI:
10.1016/j.yjmcc.2006.08.006
[Indexed for MEDLINE]
Free PMC Article
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