ArticlePloS one2020
Microvasculopathy and soft tissue calcification in mice are governed by fetuin-A, magnesium and pyrophosphate.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 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
- The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026Review
- Soft tissue accumulations of phosphate are not always associated with serum phosphate or with calcifications in mouse models of hyperphosphatemia.The Journal of physiology · 2025Article
- Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025Review
- The formation and function of calciprotein particles.Pflugers Archiv : European journal of physiology · 2025Review
- Calciprotein particles induce arterial stiffening ex vivo and impair vascular cell function.Communications biology · 2024Article
- A new perspective on intervertebral disc calcification-from bench to bedside.Bone research · 2024Review
- Weighing the Evidence for the Roles of Plasma Versus Local Pyrophosphate in Ectopic Calcification Disorders.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Biomineralogical signatures of breast microcalcifications.Science advances · 2023Article
- Review
- Increased UHMWPE Particle-Induced Osteolysis in Fetuin-A-Deficient Mice.Journal of functional biomaterials · 2023Article
- Application of the mineral-binding protein fetuin-A for the detection of calcified lesions.Theranostics · 2023Article
- Tissue chaperoning-the expanded functions of fetuin-A beyond inhibition of systemic calcification.Pflugers Archiv : European journal of physiology · 2022Review
- Level of Serum Fetuin-A Correlates with Heart Rate in Obstructive Sleep Apnea Patients without Metabolic and Cardiovascular Comorbidities.International journal of environmental research and public health · 2022Article
- Sclerostin Protects Against Vascular Calcification Development in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Risk factors and implications associated with renal mineralization in chronic kidney disease in cats.Journal of veterinary internal medicine · 2022Article
- Article
- Biomolecules Orchestrating Cardiovascular Calcification.Biomolecules · 2021Review
- In Vitro Investigation on Degradable Mg-Based Biomaterial under the Impact of the Serum Glycoprotein Fetuin.Materials (Basel, Switzerland) · 2021Article
- Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcifications can disrupt organ function in the cardiovascular system and the kidney, and are particularly common in patients with chronic kidney disease (CKD). Fetuin-A deficient mice maintained against the genetic background DBA/2 exhibit particularly severe soft tissue calcifications, while fetuin-A deficient C57BL/6 mice remain healthy. We employed molecular genetic analysis to identify risk factors of calcification in fetuin-A deficient mice. We sought to identify pharmaceutical therapeutic targets that could be influenced by dietary of parenteral supplementation. We studied the progeny of an intercross of fetuin-A deficient DBA/2 and C57BL/6 mice to identify candidate risk genes involved in calcification. We determined that a hypomorphic mutation of the Abcc6 gene, a liver ATP transporter supplying systemic pyrophosphate, and failure to regulate the Trpm6 magnesium transporter in kidney were associated with severity of calcification. Calcification prone fetuin-A deficient mice were alternatively treated with parenteral administration of fetuin-A dietary magnesium supplementation, phosphate restriction, or by or parenteral pyrophosphate. All treatments markedly reduced soft tissue calcification, demonstrated by computed tomography, histology and tissue calcium measurement. We show that pathological ectopic calcification in fetuin-A deficient DBA/2 mice is caused by a compound deficiency of three major extracellular and systemic inhibitors of calcification, namely fetuin-A, magnesium, and pyrophosphate. All three of these are individually known to contribute to stabilize protein-mineral complexes and thus inhibit mineral precipitation from extracellular fluid. We show for the first time a compound triple deficiency that can be treated by simple dietary or parenteral supplementation. This is of special importance in patients with advanced CKD, who commonly exhibit reduced serum fetuin-A, magnesium and pyrophosphate levels.
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