Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update
© 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 cond...
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th-cmuir.6653943832-588482018-09-05T04:33:58Z Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update Richard Gordan Suwakon Wongjaikam Judith K. Gwathmey Nipon Chattipakorn Siriporn C. Chattipakorn Lai Hua Xie Medicine © 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. 2018-09-05T04:33:58Z 2018-09-05T04:33:58Z 2018-09-01 Journal 15737322 13824147 2-s2.0-85045726257 10.1007/s10741-018-9700-5 https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85045726257&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/58848 |
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Medicine Richard Gordan Suwakon Wongjaikam Judith K. Gwathmey Nipon Chattipakorn Siriporn C. Chattipakorn Lai Hua Xie Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update |
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© 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. |
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Journal |
author |
Richard Gordan Suwakon Wongjaikam Judith K. Gwathmey Nipon Chattipakorn Siriporn C. Chattipakorn Lai Hua Xie |
author_facet |
Richard Gordan Suwakon Wongjaikam Judith K. Gwathmey Nipon Chattipakorn Siriporn C. Chattipakorn Lai Hua Xie |
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Richard Gordan |
title |
Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update |
title_short |
Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update |
title_full |
Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update |
title_fullStr |
Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update |
title_full_unstemmed |
Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update |
title_sort |
involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update |
publishDate |
2018 |
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https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85045726257&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/58848 |
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