Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Standard

Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction. / Stride, Nis; Larsen, Steen; Hey-Mogensen, Martin; Sander, Kåre; Lund, Jens T; Gustafsson, Finn; Køber, Lars; Dela, Flemming.

I: European Journal of Heart Failure, Bind 15, Nr. 2, 02.2013, s. 150-7.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Stride, N, Larsen, S, Hey-Mogensen, M, Sander, K, Lund, JT, Gustafsson, F, Køber, L & Dela, F 2013, 'Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction', European Journal of Heart Failure, bind 15, nr. 2, s. 150-7. https://doi.org/10.1093/eurjhf/hfs172

APA

Stride, N., Larsen, S., Hey-Mogensen, M., Sander, K., Lund, J. T., Gustafsson, F., Køber, L., & Dela, F. (2013). Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction. European Journal of Heart Failure, 15(2), 150-7. https://doi.org/10.1093/eurjhf/hfs172

Vancouver

Stride N, Larsen S, Hey-Mogensen M, Sander K, Lund JT, Gustafsson F o.a. Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction. European Journal of Heart Failure. 2013 feb.;15(2):150-7. https://doi.org/10.1093/eurjhf/hfs172

Author

Stride, Nis ; Larsen, Steen ; Hey-Mogensen, Martin ; Sander, Kåre ; Lund, Jens T ; Gustafsson, Finn ; Køber, Lars ; Dela, Flemming. / Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction. I: European Journal of Heart Failure. 2013 ; Bind 15, Nr. 2. s. 150-7.

Bibtex

@article{3be0b3ec1de34a38897154c2122d6229,
title = "Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction",
abstract = "Heart failure (HF) with left ventricular systolic dysfunction (LVSD) is associated with a shift in substrate utilization and a compromised energetic state. Whether these changes are connected with mitochondrial dysfunction is not known. We hypothesized that the cardiac phenotype in LVSD could be caused by reduced mitochondrial oxidative phosphorylation (OXPHOS) capacity and reduced mitochondrial creatine kinase (miCK) capacity. The study aim was to test mitochondrial OXPHOS capacity in LVSD myocardium compared with OXPHOS capacity in a comparable patient group without LVSD.",
author = "Nis Stride and Steen Larsen and Martin Hey-Mogensen and K{\aa}re Sander and Lund, {Jens T} and Finn Gustafsson and Lars K{\o}ber and Flemming Dela",
year = "2013",
month = feb,
doi = "10.1093/eurjhf/hfs172",
language = "English",
volume = "15",
pages = "150--7",
journal = "European Journal of Heart Failure",
issn = "1567-4215",
publisher = "JohnWiley & Sons Ltd",
number = "2",

}

RIS

TY - JOUR

T1 - Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction

AU - Stride, Nis

AU - Larsen, Steen

AU - Hey-Mogensen, Martin

AU - Sander, Kåre

AU - Lund, Jens T

AU - Gustafsson, Finn

AU - Køber, Lars

AU - Dela, Flemming

PY - 2013/2

Y1 - 2013/2

N2 - Heart failure (HF) with left ventricular systolic dysfunction (LVSD) is associated with a shift in substrate utilization and a compromised energetic state. Whether these changes are connected with mitochondrial dysfunction is not known. We hypothesized that the cardiac phenotype in LVSD could be caused by reduced mitochondrial oxidative phosphorylation (OXPHOS) capacity and reduced mitochondrial creatine kinase (miCK) capacity. The study aim was to test mitochondrial OXPHOS capacity in LVSD myocardium compared with OXPHOS capacity in a comparable patient group without LVSD.

AB - Heart failure (HF) with left ventricular systolic dysfunction (LVSD) is associated with a shift in substrate utilization and a compromised energetic state. Whether these changes are connected with mitochondrial dysfunction is not known. We hypothesized that the cardiac phenotype in LVSD could be caused by reduced mitochondrial oxidative phosphorylation (OXPHOS) capacity and reduced mitochondrial creatine kinase (miCK) capacity. The study aim was to test mitochondrial OXPHOS capacity in LVSD myocardium compared with OXPHOS capacity in a comparable patient group without LVSD.

U2 - 10.1093/eurjhf/hfs172

DO - 10.1093/eurjhf/hfs172

M3 - Journal article

C2 - 23115323

VL - 15

SP - 150

EP - 157

JO - European Journal of Heart Failure

JF - European Journal of Heart Failure

SN - 1567-4215

IS - 2

ER -

ID: 44914716