ArticleExperimental cell research2015
Phosphate uptake-independent signaling functions of the type III sodium-dependent phosphate transporter, PiT-1, in vascular smooth muscle cells.
Article in Experimental cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 98 citations in OpenAlex.
- Targeting calciphylaxis: the emergence of vitamin K as a potential treatment.Clinical kidney journal · 2026Review
- The Role and Mechanism of Gut Microbiota and Metabolites in Vascular Calcification.International journal of molecular sciences · 2026Review
- The Role of Downstream Kynurenine Pathway Metabolites in the Modulation of Cardiovascular Disease Development in Chronic Kidney Disease.International journal of tryptophan research : IJTR · 2026Review
- Calcimimetics and CaSR signaling in CKD-MBD: bone-immune-vascular crosstalk and therapeutic potential.Frontiers in immunology · 2026Review
- Decoding the regulatory role of noncoding RNAs in biological and vascular calcification.Molecular biology reports · 2025Review
- Zinc alleviates vascular calcification by activating ERK1/2-mediated autophagy.Scientific reports · 2025Article
- Osteoblasts sense extracellular levels of phosphate to control the local expression of phosphatases for matrix mineralisation.Bone reports · 2025Article
- Phosphate in Physiological and Pathological Mineralization: Important yet Often Unheeded.MedComm · 2025Review
- A new SOFrontiers in physiology · 2025Article
- Phosphate overload via the type III Na-dependent Pi transporter represses aortic wall elastic fiber formation.Fujita medical journal · 2024Article
- SGK3 promotes vascular calcification via Pit-1 in chronic kidney disease.Theranostics · 2024Article
- Key regulators of vascular calcification in chronic kidney disease: Hyperphosphatemia, BMP2, and RUNX2.PeerJ · 2024Review
- Similarities and Differences of Vascular Calcification in Diabetes and Chronic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Regulatory effects of nutritional and metabolic disorders on vascular calcification in chronic kidney disease: a narrative review.Annals of translational medicine · 2023Review
- KAP1 modulates osteogenic differentiation via the ERK/Runx2 cascade in vascular smooth muscle cells.Molecular biology reports · 2023Article
- The Pathology of Primary Familial Brain Calcification: Implications for Treatment.Neuroscience bulletin · 2023Review
- Impact of Transferrin Saturation and Anemia on Radial Artery Calcification in Patients with End-Stage Kidney Disease.Nutrients · 2022Article
- Protective Roles of Xenotropic and Polytropic Retrovirus Receptor 1 (XPR1) in Uremic Vascular Calcification.Calcified tissue international · 2022Article
- Article
- Oxidative Stress Related to Plasmalemmal and Mitochondrial Phosphate Transporters in Vascular Calcification.Antioxidants (Basel, Switzerland) · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Vascular calcification (VC) is prevalent in chronic kidney disease and elevated serum inorganic phosphate (Pi) is a recognized risk factor. The type III sodium-dependent phosphate transporter, PiT-1, is required for elevated Pi-induced osteochondrogenic differentiation and matrix mineralization in vascular smooth muscle cells (VSMCs). However, the molecular mechanism(s) by which PiT-1 promotes these processes is unclear. In the present study, we confirmed that the Pi concentration required to induce osteochondrogenic differentiation and matrix mineralization of mouse VSMCs was well above that required for maximal Pi uptake, suggesting a signaling function of PiT-1 that was independent of Pi transport. Elevated Pi-induced signaling via ERK1/2 phosphorylation was abrogated in PiT-1 deficient VSMCs, but could be rescued by wild-type (WT) and a Pi transport-deficient PiT-1 mutant. Furthermore, both WT and transport-deficient PiT-1 mutants promoted osteochondrogenic differentiation as measured by decreased SM22α and increased osteopontin mRNA expression. Finally, compared to vector alone, expression of transport-deficient PiT-1 mutants promoted VSMC matrix mineralization, but not to the extent observed with PiT-1 WT. These data suggest that both Pi uptake-dependent and -independent functions of PiT-1 are important for VSMC processes mediating vascular calcification.
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