Myocardial iron homeostasis and hepcidin expression in a rat model of heart failure at different levels of dietary iron intake
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
30677469
DOI
10.1016/j.bbagen.2019.01.010
PII: S0304-4165(19)30016-9
Knihovny.cz E-resources
- MeSH
- Administration, Oral MeSH
- Iron Deficiencies MeSH
- Iron, Dietary administration & dosage MeSH
- Hepcidins metabolism MeSH
- Homeostasis MeSH
- Rats MeSH
- Disease Models, Animal * MeSH
- Myocardium chemistry metabolism MeSH
- Rats, Sprague-Dawley MeSH
- Heart Failure metabolism MeSH
- Iron metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Iron, Dietary MeSH
- Hepcidins MeSH
- Iron MeSH
BACKGROUND: Up to 50% of patients with chronic heart failure (HF) have systemic iron deficiency, which contributes to symptoms and poor prognosis. Myocardial iron deficiency (MID) in HF patients has been recently documented, but its causes and consequences are unknown. The goal of our study was to address these questions in a well-defined rat HF model induced by volume overload due to aorto-caval fistula. METHODS: Modulation of dietary iron content in a rat model of HF has been used to address how iron status affects cardiac iron levels, heart structure and function, and how the presence of HF affects cardiac expression of hepcidin and other iron-related genes. RESULTS: MID developed in the rat model of heart failure. Iron supplementation did not normalize the myocardial iron content; however, it improved survival of HF animals compared to animals fed diet with normal iron content. We observed marked upregulation of hepcidin mRNA expression in HF animals, which was not associated with systemic or cardiac iron levels but strongly correlated with markers and parameters of heart injury. Identical iron-independent pattern was observed for expression of several iron-related genes. CONCLUSIONS: MID is not caused by defective iron absorption or decreased systemic iron levels, but rather by intrinsic myocardial iron deregulation. Altered cardiac expression of hepcidin and other iron-related genes is driven by iron-independent stimuli in the failing heart. GENERAL SIGNIFICANCE: Understanding of the causes and consequences of MID is critical for finding strategies how to improve cardiac iron stores and in HF patients.
BIOCEV 1st Faculty of Medicine Charles University Vestec Czech Republic
Institute for Clinical and Experimental Medicine IKEM Prague Czech Republic
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