ArticleCell cycle (Georgetown, Tex.)2014
Juxta-articular joint-capsule mineralization in CD73 deficient mice: similarities to patients with NT5E mutations.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 52 citations in OpenAlex.
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- Rapamycin Reduces Mineral Density and Promotes Beneficial Vascular Remodeling in a Murine Model of Severe Medial Arterial Calcification.bioRxiv : the preprint server for biology · 2025Article
- Adenosine metabolism and receptors in aging of the skin, musculoskeletal, immune and cardiovascular systems.Ageing research reviews · 2025Review
- The Purinergic Nature of Pseudoxanthoma Elasticum.Biology · 2024Review
- Inborn Errors of Purine Salvage and Catabolism.Metabolites · 2023Review
- Role of the extracellular ATP/pyrophosphate metabolism cycle in vascular calcification.Purinergic signalling · 2023Review
- 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
- INZ-701, a recombinant ENPP1 enzyme, prevents ectopic calcification in an Abcc6Experimental dermatology · 2022Article
- Inorganic Pyrophosphate Deficiency Syndromes and Potential Treatments for Pathologic Tissue Calcification.The American journal of pathology · 2022Review
- Inorganic pyrophosphate is reduced in patients with systemic sclerosis.Rheumatology (Oxford, England) · 2022Article
- Medial Arterial Calcification: A Significant and Independent Contributor of Peripheral Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Biomolecules Orchestrating Cardiovascular Calcification.Biomolecules · 2021Review
- Molecular Genetics and Modifier Genes in Pseudoxanthoma Elasticum, a Heritable Multisystem Ectopic Mineralization Disorder.The Journal of investigative dermatology · 2021Review
- ABCC6, Pyrophosphate and Ectopic Calcification: Therapeutic Solutions.International journal of molecular sciences · 2021Review
- Therapeutics Development for Pseudoxanthoma Elasticum and Related Ectopic Mineralization Disorders: Update 2020.Journal of clinical medicine · 2020Review
- Calcinosis in Systemic Sclerosis: Updates in Pathophysiology, Evaluation, and Treatment.Current rheumatology reports · 2020Review
- Dysregulation of FOXO1 (Forkhead Box O1 Protein) Drives Calcification in Arterial Calcification due to Deficiency of CD73 and Is Present in Peripheral Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Retinoids: Dissolving the Calcification Paradox.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Dysregulation of ectonucleotidase-mediated extracellular adenosine during postmenopausal bone loss.Science advances · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Arterial calcification due to CD73 deficiency (ACDC), an autosomal recessive disorder, manifests with extensive mineralization of the lower-extremity arteries as well as of hand and foot joint-capsules. This disease is caused by mutations in the NT5E gene which encodes CD73, a membrane-bound ecto-5'-nucleotidase hydrolyzing 5'-AMP into adenosine and Pi. To gain insight into the pathophysiologic details of ACDC, we have characterized a Nt5e(-/-) knock out mouse (Nt5e(tm1Jgsc)) deficient in CD73. These mice, when maintained on appropriate strain background, demonstrated stiffening of the joints and micro CT revealed distinct changes in the thoracic skeletal structure with evidence of mineralization at the costochondral junctions. Mineralization was also noted in the juxta-articular spaces of the lower extremities as well as of ligaments and capsules adjacent to the bony structures. No evidence of vascular mineralization was noted either by CT or by microdissection of arteries in the thoracic area or in lower extremities. The Nt5e(-/-) mutant mice demonstrated significantly increased Pi levels in the serum and significantly reduced PPi concentration in the heparinized plasma, resulting in markedly increased Pi/PPi ratio, thus creating a pro-mineralization environment. In conclusion, the Nt5e(-/-) targeted mutant mice recapitulate some, but not all, features of ACDC and serve as a model system to study pharmacologic interventions for ectopic mineralization. Collectively, this mouse model deficient in CD73, with other targeted mutant mice with vascular mineralization, attests to the presence of a complex pro-mineralization/anti-mineralization network that under physiologic homeostatic conditions prevents ectopic tissue mineralization.
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