ArticleCardiovascular diabetology2014
Exenatide can inhibit calcification of human VSMCs through the NF-kappaB/RANKL signaling pathway.
Article in Cardiovascular diabetology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Discovery and identification of semaphorin 4D as a bioindicator of high fracture incidence in type 2 diabetic mice with glucose control.Journal of advanced research · 2026Article
- Review
- Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- Similarities and Differences of Vascular Calcification in Diabetes and Chronic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Sleeve Gastrectomy Improves Hepatic Glucose Metabolism by Downregulating FBXO2 and Activating the PI3K-AKT Pathway.International journal of molecular sciences · 2023Article
- Review
- Medical and Surgical Obesity Treatments and Atherosclerosis: Mechanisms beyond Typical Risk Factors.Current atherosclerosis reports · 2021Review
- Effect of Erythropoietin on Calcification of Vascular Smooth Muscle Cells and Its Molecular Regulatory Mechanism.Journal of cardiovascular translational research · 2021Article
- Melatonin alleviates vascular calcification and ageing through exosomal miR-204/miR-211 cluster in a paracrine manner.Journal of pineal research · 2020Article
- Both JNK1 and JNK2 Are Indispensable for Sensitized Extracellular Matrix Mineralization in IKKβ-Deficient Osteoblasts.Frontiers in endocrinology · 2020Article
- Article
- Exosomes from hyperglycemia-stimulated vascular endothelial cells contain versican that regulate calcification/senescence in vascular smooth muscle cells.Cell & bioscience · 2019Article
- The protective effects of exenatide against AGEs-induced articular matrix degradation in human primary chondrocytes.American journal of translational research · 2019Article
- Combined effects of hyperphosphatemia and hyperglycemia on the calcification of cultured human aortic smooth muscle cells.Experimental and therapeutic medicine · 2019Article
- Activation of the non-canonical NF-κB/p52 pathway in vascular endothelial cells by RANKL elicits pro-calcific signalling in co-cultured smooth muscle cells.Cellular signalling · 2018Article
- The role of OPG/RANKL in the pathogenesis of diabetic cardiovascular disease.Cardiovascular endocrinology & metabolism · 2018Review
- Molecular and clinical roles of incretin-based drugs in patients with heart failure.Heart failure reviews · 2018Review
- Physical exercise, gut, gut microbiota, and atherosclerotic cardiovascular diseases.Lipids in health and disease · 2018Review
- The Bioactive Substance Secreted by MSC Retards Mouse Aortic Vascular Smooth Muscle Cells Calcification.BioMed research international · 2018Article
- A novel role of cellular interactions in vascular calcification.Journal of translational medicine · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundArterial calcification is an important pathological change of diabetic vascular complication. Osteoblastic differentiation of vascular smooth muscle cells (VSMCs) plays an important cytopathologic role in arterial calcification. The glucagon-like peptide-1 receptor agonists (GLP-1RA), a novel type of antidiabetic drugs, exert cardioprotective effects through the GLP-1 receptor (GLP-1R). However, the question of whether or not GLP-1RA regulates osteoblastic differentiation and calcification of VSMCs has not been answered, and the associated molecular mechanisms have not been examined.
methodsCalcifying VSMCs (CVSMCs) were isolated from cultured human arterial smooth muscle cells through limiting dilution and cloning. The extent of matrix mineralization was measured by Alizarin Red S staining. Protein expression and phosphorylation were detected by Western blot. Gene expression of receptor activator of nuclear factor-κB ligand (RANKL) was silenced by small interference RNA (siRNA).
resultsExenatide, an agonist of GLP-1 receptor, attenuated β-glycerol phosphate (β-GP) induced osteoblastic differentiation and calcification of human CVSMCs in a dose- and time-dependent manner. RANKL siRNA also inhibited osteoblastic differentiation and calcification. Exenatide decreased the expression of RANKL in a dose-dependent manner. 1,25 vitD3 (an activator of RANKL) upregulated, whereas BAY11-7082 (an inhibitor of NF-κB) downregulated RANKL, alkaline phosphatase (ALP), osteocalcin (OC), and core binding factor α1 (Runx2) protein levels and reduced mineralization in human CVSMCs. Exenatide decreased p-NF-κB and increased p-AMPKα levels in human CVSMCs 48 h after treatment. Significant decrease in p-NF-κB (p-Ser(276), p-Ser(536)) level was observed in cells treated with exenatide or exenatide + BAY11-7082.
conclusionGLP-1RA exenatide can inhibit human VSMCs calcification through NF-κB/RANKL signaling.
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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 Socratic graph.