ArticleCurrent cardiology reviews2015
Vascular Calcification Revisited: A New Perspective for Phosphate Transport
Article in Current cardiology reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- PDZ domain containing protein 1 aggravates mouse vascular smooth muscle cells calcification via PDZ1 domain mediated β-catenin stabilization and nuclear translocation.Communications biology · 2025Article
- Vascular Calcification: Key Roles of Phosphate and Pyrophosphate.International journal of molecular sciences · 2021Review
- Hydrolysis of Extracellular Pyrophosphate increases in post-hemodialysis plasma.Scientific reports · 2018Article
- Etidronate prevents dystrophic cardiac calcification by inhibiting macrophage aggregation.Scientific reports · 2018Article
- Pyrophosphate Supplementation Prevents Chronic and Acute Calcification in ABCC6-Deficient Mice.The American journal of pathology · 2017Article
- Article
- Novel phosphate-activated macrophages prevent ectopic calcification by increasing extracellular ATP and pyrophosphate.PloS one · 2017Article
- [Effect of HBP-A on meniscal injury and pathological hypertrophy and calcification of the meniscus].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2016Article
- Alkalosis and Dialytic Clearance of Phosphate Increases Phosphatase Activity: A Hidden Consequence of Hemodialysis.PloS one · 2016Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated serum phosphorus has emerged as a key risk factor for pathologic calcification of cardiovascular structures, or vascular calcification (VC). To prevent the formation of calciumphosphate deposits (CPD), the body uses adenosine-5’-triphosphate (ATP) to synthesize inhibitors of calcification, including proteins and inhibitors of low molecular weight. Extracellular pyrophosphate (PPi) is a potent inhibitor of VC, which is produced during extracellular hydrolysis of ATP. Loss of function in the enzymes and transporters that are involved in the cycle of extracellular ATP, including Pi transporters, leads to excessive deposition of calcium-phosphate salts. Treatment of hyperphosphatemia with Pi-binders and Injection of exogenous PPi are the effective treatments to prevent CPD in the aortic wall. The role of sodium phosphate cotransporters in ectopic calcification is contradictory and not well defined, but their important role in the control of intracellular Pi levels and the synthesis of ATP make them an important target to study.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.