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一种对氧化还原依赖的途径,用于调节II类HDAC和心脏缩

Tetsuro Ago1, Tong Liu, Peiyong Zhai

  • 1Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, NJ 07103, USA.

Cell
|June 17, 2008
PubMed
概括

硫素1 (Trx1) 通过修改组素脱乙酶 (HDACs) 来降低心脏缩中的氧化应激. 这种氧化还原调节阻止了HDAC的核出口,为心脏病提供了一个新的治疗点.

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