ArticleCell proliferation2021
PTH-induced EndMT via miR-29a-5p/GSAP/Notch1 pathway contributed to valvular calcification in rats with CKD.
Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Vascular calcification: pathogenic mechanisms, signaling crosstalk and translational therapeutics.Signal transduction and targeted therapy · 2026Review
- Review
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Exosomal hsa-miR-299-3p from endothelium mediates high phosphorus-induced vascular calcification in mice model of CKD via phosphorylated JAK2/STAT5 pathway.Frontiers in pharmacology · 2026Article
- The gut-kidney axis in chronic kidney disease: a vicious cycle of microbial dysbiosis and uremic toxin accumulation.Frontiers in immunology · 2026Review
- Valvular calcification in chronic kidney disease: new insights from recent clinical and preclinical studies.Clinical kidney journal · 2025Article
- Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition.Cell communication and signaling : CCS · 2025Review
- The role of microRNAs in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Noncoding RNA as a crucial epigenetic modulator in the degeneration of the ligamentum flavum.Experimental & molecular medicine · 2024Review
- Current Understanding of Cardiovascular Calcification in Patients with Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Linc-ROR Modulates the Endothelial-Mesenchymal Transition of Endothelial Progenitor Cells through the miR-145/Smad3 Signaling Pathway.Physiological research · 2024Article
- Article
- D-box-binding protein alleviates vascular calcification in rats with chronic kidney disease by activating microRNA-195-5p and downregulating cyclin D1.Biomolecules & biomedicine · 2024Article
- The functional role of cellular senescence during vascular calcification in chronic kidney disease.Frontiers in endocrinology · 2024Review
- Parathyroid Hormone Induces Human Valvular Endothelial Cells Dysfunction That Impacts the Osteogenic Phenotype of Valvular Interstitial Cells.International journal of molecular sciences · 2022Article
- Post-Transcriptional Regulation of Molecular Determinants during Cardiogenesis.International journal of molecular sciences · 2022Review
- Flow-Responsive Noncoding RNAs in the Vascular System: Basic Mechanisms for the Clinician.Journal of clinical medicine · 2022Review
- The new ceRNA crosstalk between mRNAs and miRNAs in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2022Article
- The Potential of Gamma Secretase as a Therapeutic Target for Cardiac Diseases.Journal of personalized medicine · 2021Review
- Towards Personalized Therapy of Aortic Stenosis.Journal of personalized medicine · 2021Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEndothelial-to-mesenchymal transition (EndMT) is a common pathophysiology in valvular calcification (VC) among non-chronic kidney disease (CKD) patients. However, few studies were investigated in CKD-induced VC. Parathyroid hormone (PTH) was considered to be an important component of EndMT in CKD-induced cardiovascular diseases. Therefore, determining whether PTH could induce valvular EndMT and elucidating corresponding mechanism involved further study.
methodsPerforming a 5/6 nephrectomy with a high phosphorus diet was done to construct VC models in rats with CKD. miRNA sequencing was used to ascertain changes in microRNA in human umbilical vein endothelial cells (HUVECs) intervened by PTH. VC was observed by Von Kossa staining and scanning electron microscope.
resultsPTH induced valvular EndMT in VC. Global microRNA expression profiling of HUVECs was examined in PTH versus the control in vitro, in which miR-29a-5p was most notably decreased and was resumed by PTHrP(7-34) (PTH-receptor1 inhibitor). Overexpression of miR-29a-5p could inhibit PTH-induced EndMT in vitro and valvular EndMT in vivo. The dual-luciferase assay verified that γ-secretase-activating protein (GASP) served as the target of miR-29a-5p. miR-29a-5p-mimics, si-GSAP and DAPT (γ-secretase inhibitor) inhibited PTH-induced γ-secretase activation, thus blocking Notch1 pathway activation to inhibit EndMT in vitro. Moreover, Notch1 pathway activation was observed in VC. Blocking Notch1 pathway activation via AAV-miR-29a and DAPT inhibited valvular EndMT. In addition, blocking Notch1 pathway activation was also shown to alleviate VC.
conclusionPTH activates valvular EndMT via miR-29a-5p/GSAP/Notch1 pathway, which can contribute to VC in CKD rats.
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