Myocardial iron homeostasis and hepcidin expression in a rat model of heart failure at different levels of dietary iron intake

Kód výsledku v 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>

Nalezeny alternativní kódy

RIV/00216208:11110/19:10396776 RIV/61989592:15310/19:73598138 RIV/00023736:_____/19:00012558

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

Myocardial iron homeostasis and hepcidin expression in a rat model of heart failure at different levels of dietary iron intake

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Myocardial iron homeostasis and hepcidin expression in a rat model of heart failure at different levels of dietary iron intake

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30201 - Cardiac and Cardiovascular systems

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Biochimica et biophysica acta. General subjects

ISSN

0304-4165

e-ISSN

—

Svazek periodika

1863

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

703-713

Kód UT WoS článku

000460853200006

EID výsledku v databázi Scopus

2-s2.0-85060533423