Simvastatin improves mitochondrial respiration in peripheral blood cells.
Blood Platelets
/ drug effects
Cell Line
Electron Transport Complex I
/ metabolism
Electron Transport Complex IV
/ metabolism
Female
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
/ pharmacology
Hypercholesterolemia
/ drug therapy
Leukocytes, Mononuclear
/ drug effects
Male
Middle Aged
Mitochondria
/ drug effects
Oxygen Consumption
/ drug effects
Simvastatin
/ pharmacology
Superoxides
/ metabolism
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
12 10 2020
12 10 2020
Historique:
received:
24
05
2020
accepted:
21
09
2020
entrez:
13
10
2020
pubmed:
14
10
2020
medline:
29
12
2020
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 33046789
doi: 10.1038/s41598-020-73896-2
pii: 10.1038/s41598-020-73896-2
pmc: PMC7550337
doi:
Substances chimiques
Hydroxymethylglutaryl-CoA Reductase Inhibitors
0
Superoxides
11062-77-4
Simvastatin
AGG2FN16EV
Electron Transport Complex IV
EC 1.9.3.1
Electron Transport Complex I
EC 7.1.1.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
17012Références
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