ArticleRedox biology2019
Fenofibrate improves vascular endothelial function and contractility in diabetic mice.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Fenofibrate decreased microalbuminuria in the type 2 diabetes patients with hypertriglyceridemia.Lipids in health and disease · 2020Trial
- Fenofibrate attenuates the adverse effects of radiation on endothelial cells through modulation of ROS-NO signalling and inflammation.Redox biology · 2026Article
- Renal microcirculation and mechanisms in diabetic kidney disease.Frontiers in endocrinology · 2025Review
- Hepatic-vascular crosstalk via GRK2: fenofibrate improves endothelial function by restoring lipid metabolism and NO signaling in obese mice.Frontiers in physiology · 2025Article
- Anti-inflammatory role of fenofibrate in treating diseases.Biomolecules & biomedicine · 2023Review
- Ferroptosis as a potential new therapeutic target for diabetes and its complications.Endocrine connections · 2023Review
- Role of abnormal energy metabolism in the progression of chronic kidney disease and drug intervention.Renal failure · 2022Article
- Long-Term Fenofibrate Treatment Stimulates the Phenotypic Microevolution of Prostate Cancer Cells In Vitro.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Tacrolimus Causes Hypertension by Increasing Vascular Contractility via RhoA (Ras Homolog Family Member A)/ROCK (Rho-Associated Protein Kinase) Pathway in Mice.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Fibrates: A Possible Treatment Option for Patients with Abdominal Aortic Aneurysm?Biomolecules · 2022Review
- The Association of Postprandial Triglyceride Variability with Renal Dysfunction and Microalbuminuria in Patients with Type 2 Diabetic Mellitus: A Retrospective and Observational Study.Journal of diabetes research · 2022Observational
- PPARα agonist fenofibrate relieves acquired resistance to gefitinib in non-small cell lung cancer by promoting apoptosis via PPARα/AMPK/AKT/FoxO1 pathway.Acta pharmacologica Sinica · 2022Article
- Pemafibrate Prevents Rupture of Angiotensin II-Induced Abdominal Aortic Aneurysms.Frontiers in cardiovascular medicine · 2022Article
- Alleviating effects of pea peptide on oxidative stress injury induced by lead in PC12 cellsFrontiers in nutrition · 2022Article
- Activation of PPARα by Fenofibrate Attenuates the Effect of Local Heart High Dose Irradiation on the Mouse Cardiac Proteome.Biomedicines · 2021Article
- Pemafibrate, A Novel Selective Peroxisome Proliferator-Activated Receptor α Modulator, Reduces Plasma Eicosanoid Levels and Ameliorates Endothelial Dysfunction in Diabetic Mice.Journal of atherosclerosis and thrombosis · 2021Article
- Gut microbiota dependent trimethylamine N-oxide aggravates angiotensin II-induced hypertension.Redox biology · 2021Article
- Improved Endothelium-Dependent Relaxation of Thoracic Aorta in Niclosamide-Treated Diabetic Rats.Cardiovascular toxicology · 2021Article
- Acute Kidney Injury Sensitizes the Brain Vasculature to Ang II (Angiotensin II) Constriction via FGFBP1 (Fibroblast Growth Factor Binding Protein 1).Hypertension (Dallas, Tex. : 1979) · 2020Article
- New drugs are not enough‑drug repositioning in oncology: An update.International journal of oncology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fenofibrate, a peroxisome proliferator-activated receptors α (PPARα) agonist, reduces vascular complications of diabetic patients but its protective mechanisms are not fully understood. Here we tested the hypothesis that fenofibrate improves vascular endothelial dysfunction by balancing endothelium-dependent relaxation and contractility of the aorta in diabetes mellitus (DM). In streptozotocin-induced diabetic mice, eight weeks of fenofibrate treatment (100 mg/Kg/d) improved endothelium dependent relaxation in the macro- and microvessels, increased nitric oxide (NO) levels, reduced renal damage markers and effects of the vasoconstrictor prostaglandin. Levels of superoxide dismutase and catalase were both reduced and hydrogen peroxide was increased in vehicle-treated DM, but these changes were reversed by fenofibrate treatment. Vasodilation of the aorta after fenofibrate treatment was reversed by PPARα or AMPKα inhibitors. Western blots showed that fenofibrate treatment elevated PPARα expression, induced liver kinase B1 (LKB1) translocation from the nucleus to the cytoplasm and activated AMP-activated protein kinase-α (AMPKα), thus activating endothelial NO synthase (eNOS). Also, fenofibrate treatment decreased NF-κB p65 and cyclooxygenase 2 proteins in aortas. Finally, incubation with indomethacin in vitro improved aortic contractility in diabetic mice. Overall, our results show that fenofibrate treatment in diabetic mice normalizes endothelial function by balancing vascular reactivity via increasing NO production and suppressing the vasoconstrictor prostaglandin, suggesting mechanism of action of fenofibrate in mediating diabetic vascular complications.
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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.