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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

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • 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

  • 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