Department of Pharmacology, University of Athens, School of Medicine, 75 Mikras Asias Avenue, 11527 Goudi, Athens, Greece.
Heart Fail Rev. 2010 Mar;15(2):143-54. doi: 10.1007/s10741-008-9111-0. Epub 2008 Sep 5.
Viable myocardium undergoes several changes in the course of cardiac remodeling following myocardial infarction aiming to adapt the heart to the hemodynamic compromise. This response is characterized by reactivation of the fetal transcriptional program and results in cardiac dysfunction. Changes in thyroid hormone (TH)-TH receptors (TRs) axis occur in the course of post-infarction cardiac remodeling and seem to contribute to cardiac fetal phenotype. TH can "rebuild" the post-infarcted heart by preventing the fetal-like pattern of contractile proteins expression, normalizing wall tension, and optimizing cardiac chamber geometry. This effect seems to be attributed to TH pleiotropic cellular actions; TH promotes tissue growth and differentiation and favorably remodels cardiac cell while increases cellular survival upon stress. TH may constitute a new therapeutic option for mending the ischemic myocardium.
在心肌梗死后的心脏重构过程中，存活心肌会发生多种变化，旨在使心脏适应血液动力学的代偿。这种反应的特征是胎儿转录程序的重新激活，并导致心脏功能障碍。甲状腺激素（TH）-TH 受体（TR）轴在梗死后心脏重构过程中发生变化，似乎有助于心脏胎儿表型。TH 可以通过防止收缩蛋白表达的胎儿样模式、使壁张力正常化和优化心脏腔室几何形状来“重建”梗死后的心脏。这种作用似乎归因于 TH 的多效细胞作用；TH 促进组织生长和分化，有利于心脏细胞重塑，同时增加细胞在应激下的存活。TH 可能为修复缺血心肌提供新的治疗选择。
