New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?
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.
Pantos
Constantinos
C
Department of Pharmacology, University of Athens, 75 Mikras Asias Ave., 11527, Goudi, Athens, Greece. cpantos@med.uoa.gr
Mourouzis
Iordanis
I
Cokkinos
Dennis V
DV
D015897:Comorbidity; D006333:Heart Failure / Q000188:drug therapy / Q000473:pathology*; D006360:Heat-Shock Proteins; D006439:Hemodynamics; D006801:Humans; D009203:Myocardial Infarction / Q000473:pathology*; D017202:Myocardial Ischemia / Q000473:pathology*; D015425:Myocardial Reperfusion; D015398:Signal Transduction / Q000502:physiology; D013963:Thyroid Hormones / Q000502:physiology / Q000627:therapeutic use*; D013997:Time Factors; D020257:Ventricular Remodeling
D006360:Heat-Shock Proteins; D013963:Thyroid Hormones