Myocardial iron homeostasis and hepcidin expression in a rat model of heart failure at different levels of dietary iron intake
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
30677469
DOI
10.1016/j.bbagen.2019.01.010
PII: S0304-4165(19)30016-9
Knihovny.cz E-zdroje
- MeSH
- aplikace orální MeSH
- deficit železa MeSH
- dietní železo aplikace a dávkování MeSH
- hepcidiny metabolismus MeSH
- homeostáza MeSH
- krysa rodu Rattus MeSH
- modely nemocí na zvířatech * MeSH
- myokard chemie metabolismus MeSH
- potkani Sprague-Dawley MeSH
- srdeční selhání metabolismus MeSH
- železo metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- dietní železo MeSH
- hepcidiny MeSH
- železo 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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