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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 854265, 16 pages
Review Article

Role of Oxidative Stress in Thyroid Hormone-Induced Cardiomyocyte Hypertrophy and Associated Cardiac Dysfunction: An Undisclosed Story

1Department of Physiology and Cell Biology, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
2Dorothy M. Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA
3Department of Pharmacology and Toxicology, Faculty of Pharmacy, Helwan University, Cairo, Egypt

Received 1 January 2015; Accepted 7 March 2015

Academic Editor: Vladimir Jakovljevic

Copyright © 2015 Mohammad T. Elnakish et al. 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.


Cardiac hypertrophy is the most documented cardiomyopathy following hyperthyroidism in experimental animals. Thyroid hormone-induced cardiac hypertrophy is described as a relative ventricular hypertrophy that encompasses the whole heart and is linked with contractile abnormalities in both right and left ventricles. The increase in oxidative stress that takes place in experimental hyperthyroidism proposes that reactive oxygen species are key players in the cardiomyopathy frequently reported in this endocrine disorder. The goal of this review is to shed light on the effects of thyroid hormones on the development of oxidative stress in the heart along with the subsequent cellular and molecular changes. In particular, we will review the role of thyroid hormone-induced oxidative stress in the development of cardiomyocyte hypertrophy and associated cardiac dysfunction, as well as the potential effectiveness of antioxidant treatments in attenuating these hyperthyroidism-induced abnormalities in experimental animal models.