Clinical and Molecular Aspects of Iron Metabolism in Failing Myocytes

Heart failure (HF) is a common disease that causes significant limitations on the organism’s capacity and, in extreme cases, leads to death. Clinically, iron deficiency (ID) plays an essential role in heart failure by deteriorating the patient’s condition and is a prognostic marker indicating poor c...

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Main Authors: Bogna Kozłowska, Barbara Sochanowicz, Leszek Kraj, Małgorzata Palusińska, Piotr Kołsut, Łukasz Szymański, Sławomir Lewicki, Marcin Kruszewski, Marta Załęska-Kocięcka, Przemysław Leszek
Format: Article
Language:English
Published: MDPI AG 2022-08-01
Series:Life
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Online Access:https://www.mdpi.com/2075-1729/12/8/1203
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author Bogna Kozłowska
Barbara Sochanowicz
Leszek Kraj
Małgorzata Palusińska
Piotr Kołsut
Łukasz Szymański
Sławomir Lewicki
Marcin Kruszewski
Marta Załęska-Kocięcka
Przemysław Leszek
author_facet Bogna Kozłowska
Barbara Sochanowicz
Leszek Kraj
Małgorzata Palusińska
Piotr Kołsut
Łukasz Szymański
Sławomir Lewicki
Marcin Kruszewski
Marta Załęska-Kocięcka
Przemysław Leszek
author_sort Bogna Kozłowska
collection DOAJ
description Heart failure (HF) is a common disease that causes significant limitations on the organism’s capacity and, in extreme cases, leads to death. Clinically, iron deficiency (ID) plays an essential role in heart failure by deteriorating the patient’s condition and is a prognostic marker indicating poor clinical outcomes. Therefore, in HF patients, supplementation of iron is recommended. However, iron treatment may cause adverse effects by increasing iron-related apoptosis and the production of oxygen radicals, which may cause additional heart damage. Furthermore, many knowledge gaps exist regarding the complex interplay between iron deficiency and heart failure. Here, we describe the current, comprehensive knowledge about the role of the proteins involved in iron metabolism. We will focus on the molecular and clinical aspects of iron deficiency in HF. We believe that summarizing the new advances in the translational and clinical research regarding iron deficiency in heart failure should broaden clinicians’ awareness of this comorbidity.
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spelling doaj.art-d4a3b93624ca4ddf94cf20d18104282e2023-11-30T21:49:25ZengMDPI AGLife2075-17292022-08-01128120310.3390/life12081203Clinical and Molecular Aspects of Iron Metabolism in Failing MyocytesBogna Kozłowska0Barbara Sochanowicz1Leszek Kraj2Małgorzata Palusińska3Piotr Kołsut4Łukasz Szymański5Sławomir Lewicki6Marcin Kruszewski7Marta Załęska-Kocięcka8Przemysław Leszek9Department of Heart Failure and Transplantology, The Cardinal Stefan Wyszyński National Institute of Cardiology, Alpejska 42, 04-628 Warsaw, PolandCenter of Radiobiology and Biological Dosimetry, Institute of Nuclear Chemistry and Technology, Dorodna 16, 03-195 Warsaw, PolandDepartment of Oncology, Medical University of Warsaw, 1A Banacha Str., 02-097 Warsaw, PolandDepartment of Molecular Biology, Institute of Genetics and Animal Biotechnology, Polish Academy of Science, Postępu 36A, 05-552 Magdalenka, PolandDepartment of Cardiac Surgery and Transplantology, The Cardinal Stefan Wyszyński National Institute of Cardiology, Alpejska 42, 04-628 Warsaw, PolandDepartment of Molecular Biology, Institute of Genetics and Animal Biotechnology, Polish Academy of Science, Postępu 36A, 05-552 Magdalenka, PolandDepartment of Molecular Biology, Institute of Genetics and Animal Biotechnology, Polish Academy of Science, Postępu 36A, 05-552 Magdalenka, PolandCenter of Radiobiology and Biological Dosimetry, Institute of Nuclear Chemistry and Technology, Dorodna 16, 03-195 Warsaw, PolandDepartment of Heart Failure and Transplantology, The Cardinal Stefan Wyszyński National Institute of Cardiology, Alpejska 42, 04-628 Warsaw, PolandDepartment of Heart Failure and Transplantology, The Cardinal Stefan Wyszyński National Institute of Cardiology, Alpejska 42, 04-628 Warsaw, PolandHeart failure (HF) is a common disease that causes significant limitations on the organism’s capacity and, in extreme cases, leads to death. Clinically, iron deficiency (ID) plays an essential role in heart failure by deteriorating the patient’s condition and is a prognostic marker indicating poor clinical outcomes. Therefore, in HF patients, supplementation of iron is recommended. However, iron treatment may cause adverse effects by increasing iron-related apoptosis and the production of oxygen radicals, which may cause additional heart damage. Furthermore, many knowledge gaps exist regarding the complex interplay between iron deficiency and heart failure. Here, we describe the current, comprehensive knowledge about the role of the proteins involved in iron metabolism. We will focus on the molecular and clinical aspects of iron deficiency in HF. We believe that summarizing the new advances in the translational and clinical research regarding iron deficiency in heart failure should broaden clinicians’ awareness of this comorbidity.https://www.mdpi.com/2075-1729/12/8/1203heart failuremyocardial iron metabolismoxidative stressmyocardial gathering proteins expressionhuman model
spellingShingle Bogna Kozłowska
Barbara Sochanowicz
Leszek Kraj
Małgorzata Palusińska
Piotr Kołsut
Łukasz Szymański
Sławomir Lewicki
Marcin Kruszewski
Marta Załęska-Kocięcka
Przemysław Leszek
Clinical and Molecular Aspects of Iron Metabolism in Failing Myocytes
Life
heart failure
myocardial iron metabolism
oxidative stress
myocardial gathering proteins expression
human model
title Clinical and Molecular Aspects of Iron Metabolism in Failing Myocytes
title_full Clinical and Molecular Aspects of Iron Metabolism in Failing Myocytes
title_fullStr Clinical and Molecular Aspects of Iron Metabolism in Failing Myocytes
title_full_unstemmed Clinical and Molecular Aspects of Iron Metabolism in Failing Myocytes
title_short Clinical and Molecular Aspects of Iron Metabolism in Failing Myocytes
title_sort clinical and molecular aspects of iron metabolism in failing myocytes
topic heart failure
myocardial iron metabolism
oxidative stress
myocardial gathering proteins expression
human model
url https://www.mdpi.com/2075-1729/12/8/1203
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