ArticleKidney international2018
PiT-2, a type III sodium-dependent phosphate transporter, protects against vascular calcification in mice with chronic kidney disease fed a high-phosphate diet.
Article in Kidney international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 48 citations in OpenAlex.
- A robust endothelial injury model inducing medial arterial calcification in C57BL/6J mice on a standard diet.Cardiovascular diagnosis and therapy · 2026Article
- Calcific Aortopathy in Response to Aging and Injury.Circulation · 2026Review
- Medial arterial calcification in ageing and disease: current evidence and knowledge gaps.European heart journal · 2025Review
- Association of serum phosphate levels and statin use with cardiovascular events in Japanese patients on chronic haemodialysis: a post-hoc analysis of the LANDMARK trial.Clinical kidney journal · 2025Article
- Astrocytes in Primary Familial Brain Calcification (PFBC): Emphasis on the Importance of Induced Pluripotent Stem Cell-Derived Human Astrocyte Models.Advances in experimental medicine and biology · 2025Review
- Phosphate overload via the type III Na-dependent Pi transporter represses aortic wall elastic fiber formation.Fujita medical journal · 2024Article
- Similarities and Differences of Vascular Calcification in Diabetes and Chronic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Key regulators of vascular calcification in chronic kidney disease: Hyperphosphatemia, BMP2, and RUNX2.PeerJ · 2024Review
- [Ketone Body Metabolism and Renal Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Review
- Fibroblast Growth Factor 23 Neutralizing Antibody Ameliorates Abnormal Renal Phosphate Handling in Sickle Cell Disease Mice.Endocrinology · 2023Article
- Exploring molecular profiles of calcification in aortic vascular smooth muscle cells and aortic valvular interstitial cells.Journal of molecular and cellular cardiology · 2023Article
- Role of Chronic Kidney Disease (CKD)-Mineral and Bone Disorder (MBD) in the Pathogenesis of Cardiovascular Disease in CKD.Journal of atherosclerosis and thrombosis · 2023Review
- The Pathology of Primary Familial Brain Calcification: Implications for Treatment.Neuroscience bulletin · 2023Review
- Implications of Senescent Cell Burden and NRF2 Pathway in Uremic Calcification: A Translational Study.Cells · 2023Article
- Phosphate in the Context of Cognitive Impairment and Other Neurological Disorders Occurrence in Chronic Kidney Disease.International journal of molecular sciences · 2022Review
- Protective Roles of Xenotropic and Polytropic Retrovirus Receptor 1 (XPR1) in Uremic Vascular Calcification.Calcified tissue international · 2022Article
- Oxidative Stress Related to Plasmalemmal and Mitochondrial Phosphate Transporters in Vascular Calcification.Antioxidants (Basel, Switzerland) · 2022Review
- Phosphate and Cellular Senescence.Advances in experimental medicine and biology · 2022Article
- Phosphate Is a Cardiovascular Toxin.Advances in experimental medicine and biology · 2022Review
- Recent Advances in the Role of Diet in Bone and Mineral Disorders in Chronic Kidney Disease.Current osteoporosis reports · 2021Review
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6 authors at 1 institution in 1 country.
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Abstract
PiT-2, a type III sodium-dependent phosphate transporter, is a causative gene for the brain arteriolar calcification in people with familial basal ganglion calcification. Here we examined the effect of PiT-2 haploinsufficiency on vascular calcification in uremic mice using wild-type and global PiT-2 heterozygous knockout mice. PiT-2 haploinsufficiency enhanced the development of vascular calcification in mice with chronic kidney disease fed a high-phosphate diet. No differences were observed in the serum mineral biomarkers and kidney function between the wild-type and PiT-2 heterozygous knockout groups. Micro computed tomography analyses of femurs showed that haploinsufficiency of PiT-2 decreased trabecular bone mineral density in uremia. In vitro, sodium-dependent phosphate uptake was decreased in cultured vascular smooth muscle cells isolated from PiT-2 heterozygous knockout mice compared with those from wild-type mice. PiT-2 haploinsufficiency increased phosphate-induced calcification of cultured vascular smooth muscle cells compared to the wild-type. Furthermore, compared to wild-type vascular smooth muscle cells, PiT-2 deficient vascular smooth muscle cells had lower osteoprotegerin levels and increased matrix calcification, which was attenuated by osteoprotegerin supplementation. Thus, PiT-2 in vascular smooth muscle cells protects against phosphate-induced vascular calcification and may be a therapeutic target in the chronic kidney disease population.
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