Thioredoxin and ventricular remodeling

Tetsuro Ago, Junichi Sadoshima

Research output: Contribution to journalReview articlepeer-review

74 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)762-773
Number of pages12
JournalJournal of Molecular and Cellular Cardiology
Issue number5
StatePublished - Nov 2006

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


  • Antioxidants
  • Cardiac hypertrophy
  • Heart failure
  • Ischemic heart disease
  • Reactive oxygen species
  • Thioredoxin
  • Ventricular remodeling


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