Simvastatin improves mitochondrial respiration in peripheral blood cells

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Standard

Simvastatin improves mitochondrial respiration in peripheral blood cells. / Durhuus, Jon Ambæk; Hansson, Svenja; Morville, Thomas; Kuhlman, Anja Birk; Dohlmann, Tine Lovsø; Larsen, Steen; Helge, Jørn Wulff; Angleys, Maria; Muniesa-Vargas, Alba; Bundgaard, Jens R.; Hickson, Ian David; Dela, Flemming; Desler, Claus; Rasmussen, Lene Juel.

I: Scientific Reports, Bind 10, Nr. 1, 17012, 2020.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Durhuus, JA, Hansson, S, Morville, T, Kuhlman, AB, Dohlmann, TL, Larsen, S, Helge, JW, Angleys, M, Muniesa-Vargas, A, Bundgaard, JR, Hickson, ID, Dela, F, Desler, C & Rasmussen, LJ 2020, 'Simvastatin improves mitochondrial respiration in peripheral blood cells', Scientific Reports, bind 10, nr. 1, 17012. https://doi.org/10.1038/s41598-020-73896-2

APA

Durhuus, J. A., Hansson, S., Morville, T., Kuhlman, A. B., Dohlmann, T. L., Larsen, S., Helge, J. W., Angleys, M., Muniesa-Vargas, A., Bundgaard, J. R., Hickson, I. D., Dela, F., Desler, C., & Rasmussen, L. J. (2020). Simvastatin improves mitochondrial respiration in peripheral blood cells. Scientific Reports, 10(1), [17012]. https://doi.org/10.1038/s41598-020-73896-2

Vancouver

Durhuus JA, Hansson S, Morville T, Kuhlman AB, Dohlmann TL, Larsen S o.a. Simvastatin improves mitochondrial respiration in peripheral blood cells. Scientific Reports. 2020;10(1). 17012. https://doi.org/10.1038/s41598-020-73896-2

Author

Durhuus, Jon Ambæk ; Hansson, Svenja ; Morville, Thomas ; Kuhlman, Anja Birk ; Dohlmann, Tine Lovsø ; Larsen, Steen ; Helge, Jørn Wulff ; Angleys, Maria ; Muniesa-Vargas, Alba ; Bundgaard, Jens R. ; Hickson, Ian David ; Dela, Flemming ; Desler, Claus ; Rasmussen, Lene Juel. / Simvastatin improves mitochondrial respiration in peripheral blood cells. I: Scientific Reports. 2020 ; Bind 10, Nr. 1.

Bibtex

@article{3238aa65e01f4b3d82701d27fc55f210,
title = "Simvastatin improves mitochondrial respiration in peripheral blood cells",
abstract = "Statins are prescribed to treat hypercholesterolemia and to reduce the risk of cardiovascular disease. However, statin users frequently report myalgia, which can discourage physical activity or cause patients to discontinue statin use, negating the potential benefit of the treatment. Although a proposed mechanism responsible for Statin-Associated Myopathy (SAM) suggests a correlation with impairment of mitochondrial function, the relationship is still poorly understood. Here, we provide evidence that long-term treatment of hypercholesterolemic patients with Simvastatin at a therapeutic dose significantly display increased mitochondrial respiration in peripheral blood mononuclear cells (PBMCs), and platelets compared to untreated controls. Furthermore, the amount of superoxide is higher in mitochondria in PBMCs, and platelets from Simvastatin-treated patients than in untreated controls, and the abundance of mitochondrial superoxide, but not mitochondrial respiration trends with patient-reported myalgia. Ubiquinone (also known as coenzyme Q10) has been suggested as a potential treatment for SAM; however, an 8-week course of oral ubiquinone had no impact on mitochondrial functions or the abundance of superoxide in mitochondria from PBMCs, and platelets. These results demonstrate that long-term treatment with Simvastatin increases respiration and the production of superoxide in mitochondria of PBMCs and platelets.",
author = "Durhuus, {Jon Amb{\ae}k} and Svenja Hansson and Thomas Morville and Kuhlman, {Anja Birk} and Dohlmann, {Tine Lovs{\o}} and Steen Larsen and Helge, {J{\o}rn Wulff} and Maria Angleys and Alba Muniesa-Vargas and Bundgaard, {Jens R.} and Hickson, {Ian David} and Flemming Dela and Claus Desler and Rasmussen, {Lene Juel}",
year = "2020",
doi = "10.1038/s41598-020-73896-2",
language = "English",
volume = "10",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Simvastatin improves mitochondrial respiration in peripheral blood cells

AU - Durhuus, Jon Ambæk

AU - Hansson, Svenja

AU - Morville, Thomas

AU - Kuhlman, Anja Birk

AU - Dohlmann, Tine Lovsø

AU - Larsen, Steen

AU - Helge, Jørn Wulff

AU - Angleys, Maria

AU - Muniesa-Vargas, Alba

AU - Bundgaard, Jens R.

AU - Hickson, Ian David

AU - Dela, Flemming

AU - Desler, Claus

AU - Rasmussen, Lene Juel

PY - 2020

Y1 - 2020

N2 - Statins are prescribed to treat hypercholesterolemia and to reduce the risk of cardiovascular disease. However, statin users frequently report myalgia, which can discourage physical activity or cause patients to discontinue statin use, negating the potential benefit of the treatment. Although a proposed mechanism responsible for Statin-Associated Myopathy (SAM) suggests a correlation with impairment of mitochondrial function, the relationship is still poorly understood. Here, we provide evidence that long-term treatment of hypercholesterolemic patients with Simvastatin at a therapeutic dose significantly display increased mitochondrial respiration in peripheral blood mononuclear cells (PBMCs), and platelets compared to untreated controls. Furthermore, the amount of superoxide is higher in mitochondria in PBMCs, and platelets from Simvastatin-treated patients than in untreated controls, and the abundance of mitochondrial superoxide, but not mitochondrial respiration trends with patient-reported myalgia. Ubiquinone (also known as coenzyme Q10) has been suggested as a potential treatment for SAM; however, an 8-week course of oral ubiquinone had no impact on mitochondrial functions or the abundance of superoxide in mitochondria from PBMCs, and platelets. These results demonstrate that long-term treatment with Simvastatin increases respiration and the production of superoxide in mitochondria of PBMCs and platelets.

AB - Statins are prescribed to treat hypercholesterolemia and to reduce the risk of cardiovascular disease. However, statin users frequently report myalgia, which can discourage physical activity or cause patients to discontinue statin use, negating the potential benefit of the treatment. Although a proposed mechanism responsible for Statin-Associated Myopathy (SAM) suggests a correlation with impairment of mitochondrial function, the relationship is still poorly understood. Here, we provide evidence that long-term treatment of hypercholesterolemic patients with Simvastatin at a therapeutic dose significantly display increased mitochondrial respiration in peripheral blood mononuclear cells (PBMCs), and platelets compared to untreated controls. Furthermore, the amount of superoxide is higher in mitochondria in PBMCs, and platelets from Simvastatin-treated patients than in untreated controls, and the abundance of mitochondrial superoxide, but not mitochondrial respiration trends with patient-reported myalgia. Ubiquinone (also known as coenzyme Q10) has been suggested as a potential treatment for SAM; however, an 8-week course of oral ubiquinone had no impact on mitochondrial functions or the abundance of superoxide in mitochondria from PBMCs, and platelets. These results demonstrate that long-term treatment with Simvastatin increases respiration and the production of superoxide in mitochondria of PBMCs and platelets.

U2 - 10.1038/s41598-020-73896-2

DO - 10.1038/s41598-020-73896-2

M3 - Journal article

C2 - 33046789

AN - SCOPUS:85092466764

VL - 10

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 17012

ER -

ID: 250815004