ArticlePloS one2017
Dipeptidyl peptidase-4 inhibitor gemigliptin protects against vascular calcification in an experimental chronic kidney disease and vascular smooth muscle cells.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Effect of Dipeptidyl Peptidase-4 (DPP-4) Inhibition on Biomarkers of Kidney Injury and Vascular Calcification in Diabetic Kidney Disease: A Randomized Controlled Trial.Journal of diabetes research · 2021Trial
- A prospective cohort study on effects of gemigliptin on cardiovascular outcomes in patients with type 2 diabetes (OPTIMUS study).Scientific reports · 2020Trial
- Hyperphosphataemia and NADPH Oxidase Regulation in Pathophysiological Processes: Implications for Oxidative Stress and Disease Progression.Antioxidants (Basel, Switzerland) · 2025Review
- THRA1/PGC-1α/SIRT3 pathway regulates oxidative stress and is implicated in hypertension of maternal hypothyroid rat offspring.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Antioxidative Potentials of Incretin-Based Medications: A Review of Molecular Mechanisms.Oxidative medicine and cellular longevity · 2021Review
- Pleiotropic Benefits of DPP-4 Inhibitors Beyond Glycemic Control.Clinical medicine insights. Endocrinology and diabetes · 2021Review
- Conditioned Media of Choroid Plexus Epithelium Cells Attenuates High Pi-Induced Calcification of MOVAS Cells by Inhibiting ROS-Mediated Signal Pathways.Frontiers in physiology · 2021Article
- The Role of Sclerostin in Bone and Ectopic Calcification.International journal of molecular sciences · 2020Review
- RANKL treatment of vascular endothelial cells leading to paracrine pro-calcific signaling involves ROS production.Molecular and cellular biochemistry · 2020Article
- Cardioprotection Conferred by Sitagliptin Is Associated with Reduced Cardiac Angiotensin II/Angiotensin-(1-7) Balance in Experimental Chronic Kidney Disease.International journal of molecular sciences · 2019Article
- Natural and non-natural antioxidative compounds: potential candidates for treatment of vascular calcification.Cell death discovery · 2019Review
- Adenovirus-expressing miR-153-3p alleviates aortic calcification in a rat model with chronic kidney disease.International journal of clinical and experimental pathology · 2017Article
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
Although dipeptidyl peptidase-4 inhibitors, a class of antidiabetic drugs, have various pleiotropic effects, it remains undetermined whether gemigliptin has a beneficial effect on vascular calcification. Therefore, this study was performed to evaluate the effect of gemigliptin on vascular calcification in a rat model of adenine-induced chronic kidney disease and in cultured vascular smooth muscle cells. Gemigliptin attenuated calcification of abdominal aorta and expression of RUNX2 in adenine-induced chronic kidney disease rats. In cultured vascular smooth muscle cells, phosphate-induced increase in calcium content was reduced by gemigliptin. Gemigliptin reduced phosphate-induced PiT-1 mRNA expression, reactive oxygen species generation, and NADPH oxidase mRNA expression (p22phox and NOX4). The reduction of oxidative stress by gemigliptin was associated with the downregulation of phospho-PI3K/AKT expression. High phosphate increased the expression of frizzled-3 (FDZ3) and decreased the expression of dickkopf-related protein-1 (DKK-1) in the Wnt pathway. These changes were attenuated by gemigliptin treatment. Gemigliptin restored the decreased expression of vascular smooth muscle cells markers (α-SMA and SM22α) and increased expression of osteogenic makers (CBFA1, OSX, E11, and SOST) induced by phosphate. In conclusion, gemigliptin attenuated vascular calcification and osteogenic trans-differentiation in vascular smooth muscle cells via multiple steps including downregulation of PiT-1 expression and suppression of reactive oxygen species generation, phospho-PI3K/AKT, and the Wnt signaling pathway.
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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.