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The Influence of Statins on the Aerobic Metabolism of Endothelial Cells
Endothelial mitochondrial dysfunction is considered to be the main cause of cardiovascular disease. The aim of this research was to elucidate the effects of cholesterol-lowering statins on the aerobic metabolism of endothelial cells at the cellular and mitochondrial levels. In human umbilical vein e...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073032/ https://www.ncbi.nlm.nih.gov/pubmed/32098258 http://dx.doi.org/10.3390/ijms21041485 |
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author | Broniarek, Izabela Dominiak, Karolina Galganski, Lukasz Jarmuszkiewicz, Wieslawa |
author_facet | Broniarek, Izabela Dominiak, Karolina Galganski, Lukasz Jarmuszkiewicz, Wieslawa |
author_sort | Broniarek, Izabela |
collection | PubMed |
description | Endothelial mitochondrial dysfunction is considered to be the main cause of cardiovascular disease. The aim of this research was to elucidate the effects of cholesterol-lowering statins on the aerobic metabolism of endothelial cells at the cellular and mitochondrial levels. In human umbilical vein endothelial cells (EA.hy926), six days of exposure to 100 nM atorvastatin (ATOR) induced a general decrease in mitochondrial respiration. No changes in mitochondrial biogenesis, cell viability, or ATP levels were observed, whereas a decrease in Coenzyme Q10 (Q10) content was accompanied by an increase in intracellular reactive oxygen species (ROS) production, although mitochondrial ROS production remained unchanged. The changes caused by 100 nM pravastatin were smaller than those caused by ATOR. The ATOR-induced changes at the respiratory chain level promoted increased mitochondrial ROS production. In addition to the reduced level of mitochondrial Q10, the activity of Complex III was decreased, and the amount of Complex III in a supercomplex with Complex IV was diminished. These changes may cause the observed decrease in mitochondrial membrane potential and an increase in Q10 reduction level as a consequence, leading to elevated mitochondrial ROS formation. The above observations highlight the role of endothelial mitochondria in response to potential metabolic adaptations related to the chronic exposure of endothelial cells to statins. |
format | Online Article Text |
id | pubmed-7073032 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-70730322020-03-19 The Influence of Statins on the Aerobic Metabolism of Endothelial Cells Broniarek, Izabela Dominiak, Karolina Galganski, Lukasz Jarmuszkiewicz, Wieslawa Int J Mol Sci Article Endothelial mitochondrial dysfunction is considered to be the main cause of cardiovascular disease. The aim of this research was to elucidate the effects of cholesterol-lowering statins on the aerobic metabolism of endothelial cells at the cellular and mitochondrial levels. In human umbilical vein endothelial cells (EA.hy926), six days of exposure to 100 nM atorvastatin (ATOR) induced a general decrease in mitochondrial respiration. No changes in mitochondrial biogenesis, cell viability, or ATP levels were observed, whereas a decrease in Coenzyme Q10 (Q10) content was accompanied by an increase in intracellular reactive oxygen species (ROS) production, although mitochondrial ROS production remained unchanged. The changes caused by 100 nM pravastatin were smaller than those caused by ATOR. The ATOR-induced changes at the respiratory chain level promoted increased mitochondrial ROS production. In addition to the reduced level of mitochondrial Q10, the activity of Complex III was decreased, and the amount of Complex III in a supercomplex with Complex IV was diminished. These changes may cause the observed decrease in mitochondrial membrane potential and an increase in Q10 reduction level as a consequence, leading to elevated mitochondrial ROS formation. The above observations highlight the role of endothelial mitochondria in response to potential metabolic adaptations related to the chronic exposure of endothelial cells to statins. MDPI 2020-02-21 /pmc/articles/PMC7073032/ /pubmed/32098258 http://dx.doi.org/10.3390/ijms21041485 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Broniarek, Izabela Dominiak, Karolina Galganski, Lukasz Jarmuszkiewicz, Wieslawa The Influence of Statins on the Aerobic Metabolism of Endothelial Cells |
title | The Influence of Statins on the Aerobic Metabolism of Endothelial Cells |
title_full | The Influence of Statins on the Aerobic Metabolism of Endothelial Cells |
title_fullStr | The Influence of Statins on the Aerobic Metabolism of Endothelial Cells |
title_full_unstemmed | The Influence of Statins on the Aerobic Metabolism of Endothelial Cells |
title_short | The Influence of Statins on the Aerobic Metabolism of Endothelial Cells |
title_sort | influence of statins on the aerobic metabolism of endothelial cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073032/ https://www.ncbi.nlm.nih.gov/pubmed/32098258 http://dx.doi.org/10.3390/ijms21041485 |
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