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Title: Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update
Authors: Richard Gordan
Suwakon Wongjaikam
Judith K. Gwathmey
Nipon Chattipakorn
Siriporn C. Chattipakorn
Lai Hua Xie
Keywords: Medicine
Issue Date: 1-Sep-2018
Abstract: © 2018, Springer Science+Business Media, LLC, part of Springer Nature. Iron overload cardiomyopathy (IOC) is a major cause of death in patients with diseases associated with chronic anemia such as thalassemia or sickle cell disease after chronic blood transfusions. Associated with iron overload conditions, there is excess free iron that enters cardiomyocytes through both L- and T-type calcium channels thereby resulting in increased reactive oxygen species being generated via Haber-Weiss and Fenton reactions. It is thought that an increase in reactive oxygen species contributes to high morbidity and mortality rates. Recent studies have, however, suggested that it is iron overload in mitochondria that contributes to cellular oxidative stress, mitochondrial damage, cardiac arrhythmias, as well as the development of cardiomyopathy. Iron chelators, antioxidants, and/or calcium channel blockers have been demonstrated to prevent and ameliorate cardiac dysfunction in animal models as well as in patients suffering from cardiac iron overload. Hence, either a mono-therapy or combination therapies with any of the aforementioned agents may serve as a novel treatment in iron-overload patients in the near future. In the present article, we review the mechanisms of cytosolic and/or mitochondrial iron load in the heart which may contribute synergistically or independently to the development of iron-associated cardiomyopathy. We also review available as well as potential future novel treatments.
ISSN: 15737322
Appears in Collections:CMUL: Journal Articles

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