ArticleInternational journal of molecular sciences2020
The Influence of Statins on the Aerobic Metabolism of Endothelial Cells.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Endothelial cytochrome P450 -derived cholesterol limits angiogenesis.Redox biology · 2026Article
- Association between pravastatin use and short-term mortality in ICU patients with sepsis: a retrospective propensity score-matched cohort study.Frontiers in cellular and infection microbiology · 2026Article
- Targeting TOMM40 and TOMM22 to Rescue Statin-Impaired Mitochondrial Function, Dynamics, and Mitophagy in Skeletal Myotubes.International journal of molecular sciences · 2025Article
- Adaptation of mitochondrial bioenergetics to coenzyme Q deficiency in human endothelial cells after chronic exposure to bisphosphonates.Scientific reports · 2025Article
- The bisphosphonates alendronate and zoledronate induce adaptations of aerobic metabolism in permanent human endothelial cells.Scientific reports · 2023Article
- Association of octacosanol supplementation with redox status in patients on chronic statin therapy.Journal of medical biochemistry · 2023Article
- Blocking cholesterol formation and turnover improves cellular and mitochondria function in murine heart microvascular endothelial cells and cardiomyocytes.Frontiers in physiology · 2023Article
- Mechanisms by which statins protect endothelial cells from radiation-induced injury in the carotid artery.Frontiers in cardiovascular medicine · 2023Article
- Prostate cancer cells demonstrate unique metabolism and substrate adaptability acutely after androgen deprivation therapy.The Prostate · 2022Article
- Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed.International journal of molecular sciences · 2022Review
- Effects of Endurance Training on the Coenzyme Q Redox State in Rat Heart, Liver, and Brain at the Tissue and Mitochondrial Levels: Implications for Reactive Oxygen Species Formation and Respiratory Chain Remodeling.International journal of molecular sciences · 2022Article
- Undertreatment or Overtreatment With Statins: Where Are We?Frontiers in cardiovascular medicine · 2022Review
- Protective Effects ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Article
- Improvement of Platelet Respiration by Cell-Permeable Succinate in Diabetic Patients Treated with Statins.Life (Basel, Switzerland) · 2021Article
- Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Statin Toxicity.International journal of molecular sciences · 2021Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.