title: Mitochondria as key targets of cardioprotection in cardiac ischemic disease: role of thyroid hormone triiodothyronine.
abstract: 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).
authors: CNR Institute of Clinical Physiology, Via G. Moruzzi 1, Pisa 56124, Italy. simona@ifc.cnr.it.
authors: Francesca
authors: F
authors: Forini
authors: CNR Institute of Clinical Physiology, Via G. Moruzzi 1, Pisa 56124, Italy. nicolini@ifc.cnr.it.|Tuscany Region G. Monasterio Foundation, Via G. Moruzzi 1, Pisa 56124, Italy. nicolini@ifc.cnr.it.
authors: Giuseppina
authors: G
authors: Nicolini
authors: CNR Institute of Clinical Physiology, Via G. Moruzzi 1, Pisa 56124, Italy. iervasi@ifc.cnr.it.
authors: Giorgio
authors: G
authors: Iervasi
mesh_terms: D006801:Humans; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology; D017202:Myocardial Ischemia / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D014284:Triiodothyronine / Q000378:metabolism*
chemical_list: D014284:Triiodothyronine