ArticleBritish journal of pharmacology2014
The dual PPARα/γ agonist aleglitazar increases the number and function of endothelial progenitor cells: implications for vascular function and atherogenesis.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Crosstalk along the gut-liver axis modulates glutathione and cadmium-induced hepatotoxicity.Frontiers in immunology · 2026Review
- Peroxisome Proliferator-Activated Receptor α/γ and Cannabinoid Receptor 2 Agonist Attenuated Nonalcoholic Steatohepatitis Exosome-Related Abnormalities in Mice.The American journal of pathology · 2025Article
- Anti(angiogenic) food components: can be a major source of bias in the investigation of angiogenesis inhibitors.Annals of translational medicine · 2023Review
- Whey Improves In Vitro Endothelial Mitochondrial Function and Metabolic Redox Status in Diabetic State.Antioxidants (Basel, Switzerland) · 2023Article
- Non-Alcoholic Fatty Liver Disease: Translating Disease Mechanisms into Therapeutics Using Animal Models.International journal of molecular sciences · 2023Review
- Article
- SIRT3 attenuates coronary atherosclerosis in diabetic patients by regulating endothelial cell function.Journal of clinical laboratory analysis · 2022Article
- A comparative pharmacogenomic analysis of three classic TCM prescriptions for coronary heart disease based on molecular network modeling.Acta pharmacologica Sinica · 2020Article
- Dlgap1 negatively regulates browning of white fat cells through effects on cell proliferation and apoptosis.Lipids in health and disease · 2020Article
- Endothelial Dysfunction in Diabetic Retinopathy.Frontiers in endocrinology · 2020Review
- Dual PPARα/γ agonist aleglitazar confers stroke protection in a model of mild focal brain ischemia in mice.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Anti-PCSK9 antibodies inhibit pro-atherogenic mechanisms in APOE*3Leiden.CETP mice.Scientific reports · 2019Article
- Haplotype Analysis of PPARγ Gene Polymorphisms and the Lipoprotein (a) Level.Iranian journal of public health · 2018Article
- Aleglitazar, a dual peroxisome proliferator-activated receptor-α and -γ agonist, protects cardiomyocytes against the adverse effects of hyperglycaemia.Diabetes & vascular disease research · 2017Article
- MicroRNA-27a promotes renal tubulointerstitial fibrosis via suppressing PPARγ pathway in diabetic nephropathy.Oncotarget · 2016Article
- Metformin improves the angiogenic functions of endothelial progenitor cells via activating AMPK/eNOS pathway in diabetic mice.Cardiovascular diabetology · 2016Article
- PPAR Gamma and Angiogenesis: Endothelial Cells Perspective.Journal of diabetes research · 2016Review
- Inhibition of FAAH confers increased stem cell migration via PPARα.Journal of lipid research · 2015Article
- PPARγ activation but not PPARγ haplodeficiency affects proangiogenic potential of endothelial cells and bone marrow-derived progenitors.Cardiovascular diabetology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAleglitazar is a dual PPARα/γ agonist but little is known about its effects on vascular function and atherogenesis. Hence, we characterized its effects on circulating angiogenic cells (CAC), neoangiogenesis, endothelial function, arteriogenesis and atherosclerosis in mice. EXPERIMENTAL APPROACH: C57Bl/6 wild-type (WT, normal chow), endothelial NOS (eNOS)(-/-) (normal chow) and ApoE(-/-) (Western-type diet) mice were treated with aleglitazar (10 mg·kg(-1) ·day(-1) , i.p.) or vehicle. KEY
resultsAleglitazar enhanced expression of PPARα and PPARγ target genes, normalized glucose tolerance and potently reduced hepatic fat in ApoE(-/-) mice. In WT mice, but not in eNOS(-/-) , aleglitazar up-regulated Sca-1/VEGFR2-positive CAC in the blood and bone marrow and up-regulated diLDL/lectin-positive CAC. Aleglitazar augmented CAC migration and enhanced neoangiogenesis. In ApoE(-/-) mice, aleglitazar up-regulated CAC number and function, reduced markers of vascular inflammation and potently improved perfusion restoration after hindlimb ischaemia and aortic endothelium-dependent vasodilatation. This was associated with markedly reduced formation of atherosclerotic plaques. In human cultured CAC from healthy donors and patients with coronary artery disease with or without diabetes mellitus, aleglitazar increased migration and colony-forming units in a concentration-dependent manner. Furthermore, oxidative stress-induced CAC apoptosis and expression of p53 were reduced, while telomerase activity and expression of phospho-eNOS and phospho-Akt were elevated. Comparative agonist and inhibitor experiments revealed that aleglitazar's effects on CAC migration and colony-forming units were mediated by both PPARα and PPARγ signalling and required Akt. CONCLUSIONS AND IMPLICATIONS: Aleglitazar augments the number, function and survival of CAC, which correlates with improved vascular function, enhanced arteriogenesis and prevention of atherosclerosis in mice.
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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.