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Tytuł pozycji:

Neurohormonal activation induces intracellular iron deficiency and mitochondrial dysfunction in cardiac cells

Tytuł:
Neurohormonal activation induces intracellular iron deficiency and mitochondrial dysfunction in cardiac cells
Autorzy:
M. Tajes
C. Díez-López
C. Enjuanes
P. Moliner
J. L. Ferreiro
A. Garay
S. Jiménez-Marrero
S. Yun
S. G. Sosa
L. Alcoberro
J. González-Costello
E. García-Romero
L. Yañez-Bisbe
B. Benito
J. Comín-Colet
Temat:
Neurohormonal activation
Heart failure
Iron deficiency
Cardiac cell
Mitochondria function
Biotechnology
TP248.13-248.65
Biology (General)
QH301-705.5
Biochemistry
QD415-436
Źródło:
Cell & Bioscience, Vol 11, Iss 1, Pp 1-18 (2021)
Wydawca:
BMC, 2021.
Rok publikacji:
2021
Kolekcja:
LCC:Biotechnology
LCC:Biology (General)
LCC:Biochemistry
Typ dokumentu:
article
Opis pliku:
electronic resource
Język:
English
ISSN:
2045-3701
Relacje:
https://doaj.org/toc/2045-3701
DOI:
10.1186/s13578-021-00605-5
Dostęp URL:
https://doaj.org/article/5069b2eff6f9498ca4ff3e28e7b0950a  Link otwiera się w nowym oknie
Numer akcesji:
edsdoj.5069b2eff6f9498ca4ff3e28e7b0950a
Czasopismo naukowe
Abstract Background Iron deficiency (ID) is common in patients with heart failure (HF) and is associated with poor outcomes, yet its role in the pathophysiology of HF is not well-defined. We sought to determine the consequences of HF neurohormonal activation in iron homeostasis and mitochondrial function in cardiac cells. Methods HF was induced in C57BL/6 mice by using isoproterenol osmotic pumps and embryonic rat heart-derived H9c2 cells were subsequently challenged with Angiotensin II and/or Norepinephrine. The expression of several genes and proteins related to intracellular iron metabolism were assessed by Real time-PCR and immunoblotting, respectively. The intracellular iron levels were also determined. Mitochondrial function was analyzed by studying the mitochondrial membrane potential, the accumulation of radical oxygen species (ROS) and the adenosine triphosphate (ATP) production. Results Hearts from isoproterenol-stimulated mice showed a decreased in both mRNA and protein levels of iron regulatory proteins, transferrin receptor 1, ferroportin 1 and hepcidin compared to control mice. Furthermore, mitoferrin 2 and mitochondrial ferritin were also downregulated in the hearts from HF mice. Similar data regarding these key iron regulatory molecules were found in the H9c2 cells challenged with neurohormonal stimuli. Accordingly, a depletion of intracellular iron levels was found in the stimulated cells compared to non-stimulated cells, as well as in the hearts from the isoproterenol-induced HF mice. Finally, neurohormonal activation impaired mitochondrial function as indicated by the accumulation of ROS, the impaired mitochondrial membrane potential and the decrease in the ATP levels in the cardiac cells. Conclusions HF characteristic neurohormonal activation induced changes in the regulation of key molecules involved in iron homeostasis, reduced intracellular iron levels and impaired mitochondrial function. The current results suggest that iron could be involved in the pathophysiology of HF.

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