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Oxidative Medicine and Cellular Longevity
Volume 2014, Article ID 481482, 8 pages
Review Article

The Emerging Role of TR 1 in Cardiac Repair: Potential Therapeutic Implications

Department of Pharmacology, University of Athens, 75 Mikras Asias Avenue, Goudi, 11527 Athens, Greece

Received 8 November 2013; Accepted 31 December 2013; Published 9 February 2014

Academic Editor: Neelam Khaper

Copyright © 2014 Constantinos Pantos and Iordanis Mourouzis. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Thyroid hormone (TH) is critical for adapting living organisms to environmental stress. Plasma circulating tri-iodothyronine (T3) levels drop in most disease states and are associated with increased oxidative stress. In this context, T3 levels in plasma appear to be an independent determinant for the recovery of cardiac function after myocardial infarction in patients. Thyroid hormone receptor α1 (TRα1) seems to be crucial in this response; TRα1 accumulates to cell nucleus upon activation of stress induced growth kinase signaling. Furthermore, overexpression of nuclear TRα1 in cardiomyocytes can result in pathological or physiological growth (dual action) in absence or presence of its ligand, respectively. Accordingly, inactivation of TRα1 receptor prevents reactive hypertrophy after myocardial infarction and results in heart failure with increased phospholamban (PLB) expression and marked activation of p38MAPK. In line with this evidence, TH is shown to limit ischemia/reperfusion injury and convert pathologic to physiologic growth after myocardial infarction via TRα1 receptor. TRα1 receptor may prove to be a novel pharmacological target for cardiac repair/regeneration therapies.