共 105 条
Thioredoxin1 as a negative regulator of cardiac hypertrophy
被引:48
作者:

Ago, Tetsuro
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机构:
Univ Med & Dent New Jersey, New Jersey Med Sch, Cardiovasc Res Inst, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA Univ Med & Dent New Jersey, New Jersey Med Sch, Cardiovasc Res Inst, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA

Sadoshima, Junichi
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机构:
Univ Med & Dent New Jersey, New Jersey Med Sch, Cardiovasc Res Inst, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA Univ Med & Dent New Jersey, New Jersey Med Sch, Cardiovasc Res Inst, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA
机构:
[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Cardiovasc Res Inst, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA
关键词:
D O I:
10.1089/ars.2007.1529
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
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.
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页码:679 / 687
页数:9
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