Forini Francesca, Nicolini Giuseppina, Iervasi Giorgio
CNR Institute of Clinical Physiology, Via G. Moruzzi 1, Pisa 56124, Italy.
Tuscany Region G. Monasterio Foundation, Via G. Moruzzi 1, Pisa 56124, Italy.
Int J Mol Sci. 2015 Mar 19;16(3):6312-36. doi: 10.3390/ijms16036312.
Ischemic heart disease is the major cause of mortality and morbidity worldwide. Early reperfusion after acute myocardial ischemia has reduced short-term mortality, but it is also responsible for additional myocardial damage, which in the long run favors adverse cardiac remodeling and heart failure evolution. A growing body of experimental and clinical evidence show that the mitochondrion is an essential end effector of ischemia/ reperfusion injury and a major trigger of cell death in the acute ischemic phase (up to 48-72 h after the insult), the subacute phase (from 72 h to 7-10 days) and chronic stage (from 10-14 days to one month after the insult). As such, in recent years scientific efforts have focused on mitochondria as a target for cardioprotective strategies in ischemic heart disease and cardiomyopathy. The present review discusses recent advances in this field, with special emphasis on the emerging role of the biologically active thyroid hormone triiodothyronine (T3).
缺血性心脏病是全球范围内导致死亡和发病的主要原因。急性心肌缺血后的早期再灌注降低了短期死亡率，但它也会导致额外的心肌损伤，从长远来看，这会促进不良的心脏重塑和心力衰竭的发展。越来越多的实验和临床证据表明，线粒体是缺血/再灌注损伤的关键终末效应器，也是急性缺血期（损伤后48 - 72小时内）、亚急性期（72小时至7 - 10天）和慢性期（损伤后10 - 14天至1个月）细胞死亡的主要触发因素。因此，近年来，科学研究致力于将线粒体作为缺血性心脏病和心肌病心脏保护策略的靶点。本综述讨论了该领域的最新进展，特别强调了生物活性甲状腺激素三碘甲状腺原氨酸（T3）的新作用。
