ArticleActa pharmacologica Sinica2016
Cinacalcet ameliorates aortic calcification in uremic rats via suppression of endothelial-to-mesenchymal transition.
Article in Acta pharmacologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Pooled it
- Vitamin D Deficiency and the Clinical Outcomes of Calcimimetic Therapy in Dialysis Patients: A Population-Based Study.Nutrients · 2025Article
- The Molecular Mechanisms Underlying the Systemic Effects Mediated by Parathormone in the Context of Chronic Kidney Disease.Current issues in molecular biology · 2024Review
- Short-term therapy with R568 ameliorated secondary hyperparathyroidism but does not prevent aortic valve calcification in uremic rats.Frontiers in nephrology · 2024Article
- Impact of Cinacalcet and Etelcalcetide on Bone Mineral and Cardiovascular Disease in Dialysis Patients.Current osteoporosis reports · 2023Review
- Vascular Calcification in Chronic Kidney Disease: An Update and Perspective.Aging and disease · 2022Article
- New Therapeutics Targeting Arterial Media Calcification: Friend or Foe for Bone Mineralization?Metabolites · 2022Review
- Iron, coronary artery calcification, and mortality in patients undergoing hemodialysis.Renal failure · 2021Article
- Fibroblast Growth Factor 21 Predicts and Promotes Vascular Calcification in Haemodialysis Patients.Kidney diseases (Basel, Switzerland) · 2021Article
- Review
- Crosstalk between Renal and Vascular Calcium Signaling: The Link between Nephrolithiasis and Vascular Calcification.International journal of molecular sciences · 2021Review
- Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease.Cell proliferation · 2021Review
- A Rat Model with Multivalve Calcification Induced by Subtotal Nephrectomy and High-Phosphorus Diet.Kidney diseases (Basel, Switzerland) · 2020Article
- Review
- Calcium-Sensing Receptor Participates in High Glucose-Induced EndMT in Primary Human Aortic Endothelial Cells.Frontiers in physiology · 2020Article
- Cinacalcet attenuated bone loss via inhibiting parathyroid hormone-induced endothelial-to-adipocyte transition in chronic kidney disease rats.Annals of translational medicine · 2019Article
- Endothelial to Mesenchymal Transition: Role in Physiology and in the Pathogenesis of Human Diseases.Physiological reviews · 2019Review
- The therapeutic potential of targeting the endothelial-to-mesenchymal transition.Angiogenesis · 2019Review
- Coronary flow reserve is predictive of the risk of cardiovascular death regardless of chronic kidney disease stage.Kidney 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
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimExperimental studies found that cinacalcet (CINA) markedly attenuated vascular calcification in uremic rats, but its underlying mechanisms are still largely unknown. Recent evidence have demonstrated that endothelial cells (ECs) participate in ectopic calcification in part by mediating endothelial-to-mesenchymal transition (EndMT). In this study, we investigated whether CINA ameliorated aortic calcification in uremic rats via suppression of EndMT.
methodsUremia was induced in rats by feeding rats a 0.75% adenine diet for 4 weeks. After adenine withdrawal, the rats were maintained on a 1.03% phosphorus diet for next 8 weeks. At initiation of the adenine diet, rats were orally administered CINA (10mg/kg one day) for 12 weeks. The aortic expression of EndMT- and chondrocyte- markers was examined. The effect of elevated PTH on EndMT was also studied in aortic ECs.
resultsIn uremic rats, CINA treatment significantly decreased the serum PTH concentrations, but did not affect the elevated levels of serum calcium (Ca), phosphorus (P) and Ca×P product. Besides, CINA significantly attenuated aortic calcification, and inhibited the expression of chondrocyte markers (SOX9 and COL2A1) and chondrocyte proteoglycan in uremic aortas. Moreover, CINA treatment largely abolished the up-regulation of mesenchymal markers (FSP1 and α-SMA) and down-regulation of the endothelial marker (CD31), which accompanied aortic calcification in uremic aorta samples. In vitro, PTH increased the expression of EndMT-markers in a concentration- and time-dependent manner.
conclusionThese findings suggest that strategies aiming at reducing serum PTH might prevent uremic aortic calcification by abrogating EndMT.
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