Mourouzis Iordanis, Forini Francesca, Pantos Constantinos, Iervasi Giorgio
Department of Pharmacology, University of Athens, 11527 Athens, Greece.
J Thyroid Res. 2011;2011:958626. doi: 10.4061/2011/958626. Epub 2011 Jun 19.
Nature's models of regeneration provide substantial evidence that a natural healing process may exist in the heart. Analogies existing between the damaged myocardium and the developing heart strongly indicate that regulatory factors which drive embryonic heart development may also control aspects of heart regeneration. In this context, thyroid hormone (TH) which is critical in heart maturation during development appears to have a reparative role in adult life. Thus, changes in TH -thyroid hormone receptor (TR) homeostasis are shown to govern the return of the damaged myocardium to the fetal phenotype. Accordingly, thyroid hormone treatment preferentially rebuilds the injured myocardium by reactivating developmental gene programming. Clinical data provide further support to this experimental evidence and changes in TH levels and in particular a reduction of biologically active triiodothyronine (T3) in plasma after myocardial infarction or during evolution of heart failure, are strongly correlated with patients morbidity and mortality. The potential of TH to regenerate a diseased heart has now been testing in patients with acute myocardial infarction in a phase II, randomized, double blind, placebo-controlled study (the THiRST study).
自然界的再生模型提供了大量证据，表明心脏中可能存在自然愈合过程。受损心肌与发育中的心脏之间存在的相似性有力地表明，驱动胚胎心脏发育的调节因子也可能控制心脏再生的各个方面。在这种情况下，甲状腺激素（TH）在发育过程中心脏成熟中起着关键作用，在成年期似乎具有修复作用。因此，TH-甲状腺激素受体（TR）稳态的变化被证明可控制受损心肌向胎儿表型的转变。相应地，甲状腺激素治疗通过重新激活发育基因程序，优先重建受损心肌。临床数据为这一实验证据提供了进一步支持，心肌梗死后或心力衰竭进展过程中TH水平的变化，尤其是血浆中生物活性三碘甲状腺原氨酸（T3）的降低，与患者的发病率和死亡率密切相关。目前，在一项II期随机双盲安慰剂对照研究（THiRST研究）中，已经在急性心肌梗死患者中测试了TH使患病心脏再生的潜力。
