Thioredoxin1 as a negative regulator of cardiac hypertrophy.
Excessive reactive oxygen species (ROS) play an important role in the development of cardiac hypertrophy. In contrast, antioxidants scavenge ROS, thereby maintaining the reduced environment of cells and inhibiting hypertrophy in the heart. Thioredoxin1 (Trx1) not only functions as a major antioxidant in the heart but also interacts with important signaling molecules and transcription factors, thereby attenuating cardiac hypertrophy. This review will discuss the molecular mechanisms by which Trx1 exerts antihypertrophic effects in the heart.
Ago
Tetsuro
T
Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey 07103, USA.
Sadoshima
Junichi
J
D000818:Animals; D006332:Cardiomegaly / Q000188:drug therapy* / Q000473:pathology*; D002462:Cell Membrane / Q000378:metabolism; D002467:Cell Nucleus / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D013879:Thioredoxins / Q000627:therapeutic use*
D013879:Thioredoxins