Myocardial iron homeostasis and hepcidin expression in a rat model of heart failure at different levels of dietary iron intake
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F19%3A00077676" target="_blank" >RIV/00023001:_____/19:00077676 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11110/19:10396776 RIV/61989592:15310/19:73598138 RIV/00023736:_____/19:00012558
Result on the web
<a href="https://reader.elsevier.com/reader/sd/pii/S0304416519300169?token=9F07E28FD55931EFE061E6E9934F8B0411D2E821D1A42002186458EEDFA231F58FC4200E49B02CBD2EFB8849E18D7739" target="_blank" >https://reader.elsevier.com/reader/sd/pii/S0304416519300169?token=9F07E28FD55931EFE061E6E9934F8B0411D2E821D1A42002186458EEDFA231F58FC4200E49B02CBD2EFB8849E18D7739</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.bbagen.2019.01.010" target="_blank" >10.1016/j.bbagen.2019.01.010</a>
Alternative languages
Result language
angličtina
Original language name
Myocardial iron homeostasis and hepcidin expression in a rat model of heart failure at different levels of dietary iron intake
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30201 - Cardiac and Cardiovascular systems
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2019
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Biochimica et biophysica acta. General subjects
ISSN
0304-4165
e-ISSN
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Volume of the periodical
1863
Issue of the periodical within the volume
4
Country of publishing house
US - UNITED STATES
Number of pages
11
Pages from-to
703-713
UT code for WoS article
000460853200006
EID of the result in the Scopus database
2-s2.0-85060533423