TY - JOUR
T1 - Thioredoxin and ventricular remodeling
AU - Ago, Tetsuro
AU - Sadoshima, Junichi
N1 - Funding Information:
We thank Daniela Zablocki for critical reading of the manuscript. This work was supported in part by U.S. Public Health Service Grants HL 59139, HL67724, HL67727, HL69020, and HL 73048 and by the American Heart Association grant 0340123N. T.A. is supported in part by a Research Fellowship from the Uehara Memorial Foundation, Japan.
PY - 2006/11
Y1 - 2006/11
N2 - 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.
AB - 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.
KW - Antioxidants
KW - Cardiac hypertrophy
KW - Heart failure
KW - Ischemic heart disease
KW - Reactive oxygen species
KW - Thioredoxin
KW - Ventricular remodeling
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U2 - 10.1016/j.yjmcc.2006.08.006
DO - 10.1016/j.yjmcc.2006.08.006
M3 - Review article
C2 - 17007870
AN - SCOPUS:33750384450
SN - 0022-2828
VL - 41
SP - 762
EP - 773
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
IS - 5
ER -