Thioredoxin and ventricular remodeling.

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.

journal_name

J Mol Cell Cardiol

authors

Ago T,Sadoshima J

doi

10.1016/j.yjmcc.2006.08.006

subject

Has Abstract

pub_date

2006-11-01 00:00:00

pages

762-73

issue

5

eissn

0022-2828

issn

1095-8584

pii

S0022-2828(06)00762-0

journal_volume

41

pub_type

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