Myocardial iron content and mitochondrial function in human heart failure: a direct tissue analysis

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F17%3A00060284" target="_blank" >RIV/00023001:_____/17:00060284 - isvavai.cz</a>

Alternative codes found

RIV/67985823:_____/17:00477808 RIV/00216208:11130/17:10360627 RIV/00216208:11110/17:10360627 RIV/61989592:15310/17:73583909 RIV/00064203:_____/17:10360627

Result on the web

<a href="http://onlinelibrary.wiley.com/doi/10.1002/ejhf.640/epdf" target="_blank" >http://onlinelibrary.wiley.com/doi/10.1002/ejhf.640/epdf</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/ejhf.640" target="_blank" >10.1002/ejhf.640</a>

Result language

angličtina

Original language name

Myocardial iron content and mitochondrial function in human heart failure: a direct tissue analysis

Original language description

AIMS: Iron replacement improves clinical status in iron-deficient patients with heart failure (HF), but the pathophysiology is poorly understood. Iron is essential not only for erythropoiesis, but also for cellular bioenergetics. The impact of myocardial iron deficiency (MID) on mitochondrial function, measured directly in the failing human heart, is unknown. METHODS AND RESULTS: Left ventricular samples were obtained from 91 consecutive HF patients undergoing transplantation and 38 HF-free organ donors (controls). Total myocardial iron content, mitochondrial respiration, citric acid cycle and respiratory chain enzyme activities, respiratory chain components (complex I-V), and protein content of reactive oxygen species (ROS)-protective enzymes were measured in tissue homogenates to quantify mitochondrial function. Myocardial iron content was lower in HF compared with controls (156 ± 41 vs. 200 ± 38 µg·g-1 dry weight, P &lt; 0.001), independently of anaemia. MID (the lowest iron tercile in HF) was associated with more extensive coronary disease and less beta-blocker usage compared with non-MID HF patients. Compared with controls, HF patients displayed reduced myocardial oxygen2 respiration and reduced activity of all examined mitochondrial enzymes (all P &lt; 0.001). MID in HF was associated with preserved activity of respiratory chain enzymes but reduced activity of aconitase and citrate synthase (by -26% and -15%, P &lt; 0.05) and reduced expression of catalase, glutathione peroxidase, and superoxide dismutase 2. CONCLUSION: Myocardial iron content is decreased and mitochondrial functions are impaired in advanced HF. MID in HF is associated with diminished citric acid cycle enzyme activities and decreased ROS-protecting enzymes. MID may contribute to altered myocardial substrate use and to worsening of mitochondrial dysfunction that exists in HF.

Czech name

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Czech description

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Type

J_imp - 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

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)

Publication year

2017

Confidentiality

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

Name of the periodical

European journal of heart failure

ISSN

1388-9842

e-ISSN

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Volume of the periodical

19

Issue of the periodical within the volume

4

Country of publishing house

US - UNITED STATES

Number of pages

9

Pages from-to

522-530

UT code for WoS article

000401004500011

EID of the result in the Scopus database

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