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The Scientific World Journal
Volume 2012, Article ID 741861, 17 pages
Review Article

Oxidative Stress and Heart Failure in Altered Thyroid States

1Department of Zoology, Utkal University, Odisha, Bhubaneswar 751004, India
2Department of Zoology, Ravenshaw University, Odisha, Cuttack 753003, India

Received 31 October 2011; Accepted 25 December 2011

Academic Editors: B. Biondi, L. Lanfrancone, E. Skalidis, and F. Thuny

Copyright © 2012 Pallavi Mishra and Luna Samanta. 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.


Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that hyperthyroidism induces a hyperdynamic cardiovascular state, which is associated with a faster heart rate, enhanced left ventricular systolic and diastolic function whereas hypothyroidism is characterized by the opposite changes. Hyperthyroidism and hypothyroidism represent opposite clinical conditions, albeit not mirror images. Recent experimental and clinical studies have suggested the involvement of ROS tissue damage under altered thyroid status. Altered-thyroid state-linked changes in heart modify their susceptibility to oxidants and the extent of the oxidative damage they suffer following oxidative challenge. Chronic increase in the cellular levels of ROS can lead to a catastrophic cycle of DNA damage, mitochondrial dysfunction, further ROS generation and cellular injury. Thus, these cellular events might play an important role in the development and progression of myocardial remodeling and heart failure in altered thyroid states (hypo- and hyper-thyroidism). The present review aims at elucidating the various signaling pathways mediated via ROS and their modulation under altered thyroid state and the possibility of antioxidant therapy.