Department of Pharmacology, University of Athens, 75 Mikras Asias Ave., 11527, Goudi, Athens, Greece.
Heart Fail Rev. 2011 Jan;16(1):79-96. doi: 10.1007/s10741-010-9185-3.
Chronic ischemia or pressure overload decreases thyroid hormone (TH) signaling and activates the fetal gene program in the heart. While these features are of physiologic importance in the developing heart, their respective roles in the postnatal heart are debated. Administration of TH can prevent the changes of the fetal gene program and rebuild the heart after an "index event" such as ischemia. TH affects cardiac remodeling by limiting reperfusion injury, and, at later states, by inducing distinct changes in cardiac chamber geometry in a time-dependent manner. Furthermore, administration of TH can convert pathologic to physiologic hypertrophy. These effects are the result of favorable cellular remodeling. While preliminary clinical studies provide encouraging results, the potential and efficacy of TH in the treatment of heart disease still await evaluation in large clinical trials.
慢性缺血或压力超负荷会降低甲状腺激素（TH）信号，并激活心脏中的胎儿基因程序。虽然这些特征在发育中的心脏中具有重要的生理意义，但它们在出生后心脏中的各自作用仍存在争议。TH 的给药可以防止胎儿基因程序的变化，并在“指数事件”（如缺血）后重建心脏。TH 通过限制再灌注损伤来影响心脏重构，并且在后期，通过以时间依赖性方式引起心脏腔室几何形状的不同变化。此外，TH 的给药可以将病理性肥大转化为生理性肥大。这些作用是细胞重构有利的结果。虽然初步的临床研究提供了令人鼓舞的结果，但 TH 在心脏病治疗中的潜力和疗效仍有待大型临床试验评估。
