ArticlePloS one2012
Accelerated growth plate mineralization and foreshortened proximal limb bones in fetuin-A knockout mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 60 citations in OpenAlex.
- Sustained release of exogeneous fetuin-A from Hyaluronic acid microplates decreases joint degeneration, synovial hyperplasia and muscle damage in a murine post-traumatic osteoarthritis model.Arthritis research & therapy · 2025Article
- The formation and function of calciprotein particles.Pflugers Archiv : European journal of physiology · 2025Review
- Humoral and cellular factors inhibit phosphate-induced vascular calcification during the growth period.Journal of clinical biochemistry and nutrition · 2023Article
- Increased UHMWPE Particle-Induced Osteolysis in Fetuin-A-Deficient Mice.Journal of functional biomaterials · 2023Article
- Fetuin-A is an immunomodulator and a potential therapeutic option in BMP4-dependent heterotopic ossification and associated bone mass loss.Bone research · 2022Article
- Tissue chaperoning-the expanded functions of fetuin-A beyond inhibition of systemic calcification.Pflugers Archiv : European journal of physiology · 2022Review
- Bone Biomarkers in Mucopolysaccharidoses.International journal of molecular sciences · 2021Review
- The Physiological and Pathological Role of Tissue Nonspecific Alkaline Phosphatase beyond Mineralization.Biomolecules · 2021Review
- 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
- Comparative proteomic analysis of human mesenchymal stromal cell behavior on calcium phosphate ceramics with different osteoinductive potential.Materials today. Bio · 2020Article
- Fetuin-A and fetal growth in gestational diabetes mellitus.BMJ open diabetes research & care · 2020Article
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- Fetuin-A in Infants Born Small- or Large-for-Gestational-Age.Frontiers in endocrinology · 2020Article
- The role of intra-articular administration of Fetuin-A in post-traumatic knee osteoarthritis: an experimental study in a rat model.Journal of experimental orthopaedics · 2019Article
- Chemokines in Physiological and Pathological Bone Remodeling.Frontiers in immunology · 2019Review
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- The effects of HAP and macrophage cells to the expression of inflammatory factors and apoptosis in HK-2 cells of vitro co-cultured system.Urolithiasis · 2018Article
- Article
- Surgically‑induced mouse models in the study of bone regeneration: Current models and future directions (Review).Molecular medicine reports · 2017Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The plasma protein fetuin-A/alpha2-HS-glycoprotein (genetic symbol Ahsg) is a systemic inhibitor of extraskeletal mineralization, which is best underscored by the excessive mineral deposition found in various tissues of fetuin-A deficient mice on the calcification-prone genetic background DBA/2. Fetuin-A is known to accumulate in the bone matrix thus an effect of fetuin-A on skeletal mineralization is expected. We examined the bones of fetuin-A deficient mice maintained on a C57BL/6 genetic background to avoid bone disease secondary to renal calcification. Here, we show that fetuin-A deficient mice display normal trabecular bone mass in the spine, but increased cortical thickness in the femur. Bone material properties, as well as mineral and collagen characteristics of cortical bone were unaffected by the absence of fetuin-A. In contrast, the long bones especially proximal limb bones were severely stunted in fetuin-A deficient mice compared to wildtype littermates, resulting in increased biomechanical stability of fetuin-A deficient femora in three-point-bending tests. Elevated backscattered electron signal intensities reflected an increased mineral content in the growth plates of fetuin-A deficient long bones, corroborating its physiological role as an inhibitor of excessive mineralization in the growth plate cartilage matrix--a site of vigorous physiological mineralization. We show that in the case of fetuin-A deficiency, active mineralization inhibition is a necessity for proper long bone growth.
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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.