ArticleAmerican journal of physiology. Renal physiology2017
Elevated PTH induces endothelial-to-chondrogenic transition in aortic endothelial cells.
Article in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Risk factors for coronary artery calcification in Chinese patients undergoing maintenance hemodialysis: a meta-analysis.International urology and nephrology · 2025Pooled it
- Paradox of Exercise and Coronary Artery Calcification: Potential Underlying Mechanisms.Circulation research · 2025Review
- Current Understanding of Cardiovascular Calcification in Patients with Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Hyperparathyroidism and Peripheral Arterial Disease.Current vascular pharmacology · 2024Review
- Parathyroid Hormone Induces Human Valvular Endothelial Cells Dysfunction That Impacts the Osteogenic Phenotype of Valvular Interstitial Cells.International journal of molecular sciences · 2022Article
- Article
- PTH-induced EndMT via miR-29a-5p/GSAP/Notch1 pathway contributed to valvular calcification in rats with CKD.Cell proliferation · 2021Article
- Fibroblast Growth Factor 21 Predicts and Promotes Vascular Calcification in Haemodialysis Patients.Kidney diseases (Basel, Switzerland) · 2021Article
- Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease.Cell proliferation · 2021Review
- Research Models for Studying Vascular Calcification.International journal of molecular sciences · 2020Review
- 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
- Effects of combined menaquinone-4 and PTHEndocrine · 2019Article
- Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signal-regulated protein kinase 1/2 and nuclear factor-κB signaling pathways.Experimental and therapeutic medicine · 2018Article
- Role of Vitamin D in Uremic Vascular Calcification.BioMed research international · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Previous studies have shown that increased parathyroid hormone (PTH) attributable to secondary hyperparathyroidism in chronic kidney disease accelerates the arteriosclerotic fibrosis and calcification. Although the underlying mechanisms remain largely unknown, endothelial cells (ECs) have recently been demonstrated to participate in calcification in part by providing chondrogenic cells via the endothelial-to-mesenchymal transition (EndMT). Therefore, this study aimed to investigate whether elevated PTH could induce endothelial-to-chondrogenic transition in aortic ECs and to determine the possible underlying signaling pathway. We found that treatment of ECs with PTH significantly upregulated the expression of EndMT-related markers. Accordingly, ECs treated with PTH exhibited chondrogenic potential. In vivo, lineage-tracing model-subjected mice with endothelial-specific green fluorescent protein fluorescence to chronic PTH infusion showed a marked increase in the aortic expression of chondrocyte markers, and confocal microscopy revealed the endothelial origin of cells expressing chondrocyte markers in the aorta after PTH infusion. Furthermore, this in vitro study showed that PTH enhanced the nuclear localization of β-catenin in ECs, whereas β-catenin siRNA or DKK1, an inhibitor of β-catenin nuclear translocation, attenuated the upregulation of EndMT-associated and chondrogenic markers induced by PTH. In summary, our study demonstrated that elevated PTH could induce the transition of ECs to chondrogenic cells via EndMT, possibly mediated by the nuclear translocation of β-catenin.
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Registered trials
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