ArticleJournal of diabetes research2016
Coenzyme Q10 Attenuates High Glucose-Induced Endothelial Progenitor Cell Dysfunction through AMP-Activated Protein Kinase Pathways.
Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Lipid metabolism ofWorld journal of diabetes · 2025Article
- Research Progress of Coenzyme Q in Diabetes Mellitus and Its Common Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Coenzyme Q10: A Key Antioxidant in the Management of Diabetes-Induced Cardiovascular Complications-An Overview of Mechanisms and Clinical Evidence.International journal of endocrinology · 2024Review
- Detrimental Effects of Lipid Peroxidation in Type 2 Diabetes: Exploring the Neutralizing Influence of Antioxidants.Antioxidants (Basel, Switzerland) · 2022Review
- Melatonin Improves Ischemia-Induced Circulation Recovery Impairment in Mice with Streptozotocin-Induced Diabetes by Improving the Endothelial Progenitor Cells Functioning.International journal of molecular sciences · 2022Article
- Study on the serum level of CoQ10B in patients with Moyamoya disease and its mechanism of affecting disease progression.Arquivos de neuro-psiquiatria · 2022Article
- Role of Coenzyme QAntioxidants (Basel, Switzerland) · 2021Review
- Panax quinquefolium saponin Optimizes Energy Homeostasis by Modulating AMPK-Activated Metabolic Pathways in Hypoxia-Reperfusion Induced Cardiomyocytes.Chinese journal of integrative medicine · 2021Article
- In search of elixir: Pharmacological agents against stem cell senescence.Iranian journal of basic medical sciences · 2021Review
- The Use of Coenzyme Q10 in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Endothelial progenitor cells as critical mediators of environmental air pollution-induced cardiovascular toxicity.American journal of physiology. Heart and circulatory physiology · 2021Review
- Pathophysiological Basis for Nutraceutical Supplementation in Heart Failure: A Comprehensive Review.Nutrients · 2021Review
- The proper concentrations of dextrose and lidocaine in regenerative injection therapy:The Korean journal of pain · 2021Article
- Coenzyme Q10 in association with metabolism-related AMPK/PFKFB3 and angiogenic VEGF/VEGFR2 genes in breast cancer patients.Molecular biology reports · 2020Article
- CoQ10 and Aging.Biology · 2019Review
- C3a Receptor Inhibition Protects Brain Endothelial Cells Against Oxygen-glucose Deprivation/Reperfusion.Experimental neurobiology · 2019Article
- Diabetic endothelial colony forming cells have the potential for restoration with glycomimetics.Scientific reports · 2019Article
- Overexpression of hexokinase 2 reduces mitochondrial calcium overload in coronary endothelial cells of type 2 diabetic mice.American journal of physiology. Cell physiology · 2018Article
- Reduced Vitamin D Receptor on Circulating Endothelial Progenitor Cells: A New Risk Factor of Coronary Artery Diseases.Journal of atherosclerosis and thrombosis · 2018Article
- Chronic hyperuricemia impairs blood flow recovery in the ischemic hindlimb through suppression of endothelial progenitor cells.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coenzyme Q10 (CoQ10), an antiapoptosis enzyme, is stored in the mitochondria of cells. We investigated whether CoQ10 can attenuate high glucose-induced endothelial progenitor cell (EPC) apoptosis and clarified its mechanism. EPCs were incubated with normal glucose (5 mM) or high glucose (25 mM) environment for 3 days, followed by treatment with CoQ10 (10 μM) for 24 hr. Cell proliferation, nitric oxide (NO) production, and JC-1 assay were examined. The specific signal pathways of AMP-activated protein kinase (AMPK), eNOS/Akt, and heme oxygenase-1 (HO-1) were also assessed. High glucose reduced EPC functional activities, including proliferation and migration. Additionally, Akt/eNOS activity and NO production were downregulated in high glucose-stimulated EPCs. Administration of CoQ10 ameliorated high glucose-induced EPC apoptosis, including downregulation of caspase 3, upregulation of Bcl-2, and increase in mitochondrial membrane potential. Furthermore, treatment with CoQ10 reduced reactive oxygen species, enhanced eNOS/Akt activity, and increased HO-1 expression in high glucose-treated EPCs. These effects were negated by administration of AMPK inhibitor. Transplantation of CoQ10-treated EPCs under high glucose conditions into ischemic hindlimbs improved blood flow recovery. CoQ10 reduced high glucose-induced EPC apoptosis and dysfunction through upregulation of eNOS, HO-1 through the AMPK pathway. Our findings provide a potential treatment strategy targeting dysfunctional EPC in diabetic patients.
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