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Melenovsky 2016 Eur J Heart Fail
Additional label 2016-11  +
Diseases Cardiovascular  +
Enzyme Complex I  + , Complex II;succinate dehydrogenase  + , Complex III  + , Complex IV;cytochrome c oxidase  + , Complex V;ATP synthase  +
Has abstract Iron replacement improves clinical status
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. 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 < 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 oxygen<sub>2</sub> respiration and reduced activity of all examined mitochondrial enzymes (all P < 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 < 0.05) and reduced expression of catalase, glutathione peroxidase, and superoxide dismutase 2. 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. © 2016 The Authors. European Journal of Heart Failure © 2016 European Society of Cardiology.
ure © 2016 European Society of Cardiology.  +
Has info [https://www.ncbi.nlm.nih.gov/pubmed/27647766 PMID: 27647766]  +
Has publicationkeywords Bioenergetics  + , Heart failure  + , Iron deficiency  + , Metabolism  + , Mitochondria  + , Reactive oxygen species  +
Has title Melenovsky V, Petrak J, Mracek T, Benes J,
Melenovsky V, Petrak J, Mracek T, Benes J, Borlaug BA, Nuskova H, Pluhacek T, Spatenka J, Kovalcikova J, Drahota Z, Kautzner J, Pirk J, Houstek J (2016) Myocardial iron content and mitochondrial function in human heart failure: a direct tissue analysis. Eur J Heart Fail 19:522-30.
ssue analysis. Eur J Heart Fail 19:522-30.  +
Instrument and method Oxygraph-2k  +
Mammal and model Human  +
MiP area Respiration  + , Patients  +
Pathways N  + , S  +
Preparation Homogenate  +
Tissue and cell Heart  +
Was published by MiPNetLab CZ Prague Houstek J + , CZ Prague Kalous M + , Drahota Z +
Was published in journal Eur J Heart Fail +
Was published in year 2016  +
Was written by Melenovsky V + , Petrak J + , Mracek T + , Benes J + , Borlaug BA + , Nuskova H + , Pluhacek T + , Spatenka J + , Kovalcikova J + , Drahota Z + , Kautzner J + , Pirk J + , Houstek J +
Categories Publications
Modification date
"Modification date" is a predefined property that corresponds to the date of the last modification of a subject and is provided by Semantic MediaWiki.
10:53:42, 9 November 2017  +
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