ArticleProceedings of the National Academy of Sciences of the United States of America2012
A soluble bone morphogenetic protein type IA receptor increases bone mass and bone strength.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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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Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
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- [Latest Research Findings on the Regulation of Bone Homeostasis by ALK3].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2022Review
- Functionally diverse heteromeric traps for ligands of the transforming growth factor-β superfamily.Scientific reports · 2021Article
- Smad2/3 Activation Regulates Smad1/5/8 Signaling via a Negative Feedback Loop to Inhibit 3T3-L1 Adipogenesis.International journal of molecular sciences · 2021Article
- The hepcidin regulator erythroferrone is a new member of the erythropoiesis-iron-bone circuitry.eLife · 2021Article
- Article
- Treatment with soluble bone morphogenetic protein type 1A receptor fusion protein alleviates irradiation-induced bone loss in mice through increased bone formation and reduced bone resorption.American journal of translational research · 2020Article
- The Bone Morphogenetic Protein Pathway: The Osteoclastic Perspective.Frontiers in cell and developmental biology · 2020Review
- Systemic osteoprotective effects ofChinese medicine · 2020Article
- Bone Morphogenetic Protein 4 Gene Therapy in Mice Inhibits Myeloma Tumor Growth, But Has a Negative Impact on Bone.JBMR plus · 2020Article
- Transcriptomic profiling of the myeloma bone-lining niche reveals BMP signalling inhibition to improve bone disease.Nature communications · 2019Article
- A soluble bone morphogenetic protein type 1A receptor fusion protein treatment prevents glucocorticoid-Induced bone loss in mice.American journal of translational research · 2019Article
- BMPRIA is required for osteogenic differentiation and RANKL expression in adult bone marrow mesenchymal stromal cells.Scientific reports · 2018Article
- Article
- Mechanical basis of bone strength: influence of bone material, bone structure and muscle action.Journal of musculoskeletal & neuronal interactions · 2017Review
- Strategic Targeting of Multiple BMP Receptors Prevents Trauma-Induced Heterotopic Ossification.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Article
- Bone-associated gene evolution and the origin of flight in birds.BMC genomics · 2016Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diseases such as osteoporosis are associated with reduced bone mass. Therapies to prevent bone loss exist, but there are few that stimulate bone formation and restore bone mass. Bone morphogenetic proteins (BMPs) are members of the TGFβ superfamily, which act as pleiotropic regulators of skeletal organogenesis and bone homeostasis. Ablation of the BMPR1A receptor in osteoblasts increases bone mass, suggesting that inhibition of BMPR1A signaling may have therapeutic benefit. The aim of this study was to determine the skeletal effects of systemic administration of a soluble BMPR1A fusion protein (mBMPR1A-mFc) in vivo. mBMPR1A-mFc was shown to bind BMP2/4 specifically and with high affinity and prevent downstream signaling. mBMPR1A-mFc treatment of immature and mature mice increased bone mineral density, cortical thickness, trabecular bone volume, thickness and number, and decreased trabecular separation. The increase in bone mass was due to an early increase in osteoblast number and bone formation rate, mediated by a suppression of Dickkopf-1 expression. This was followed by a decrease in osteoclast number and eroded surface, which was associated with a decrease in receptor activator of NF-κB ligand (RANKL) production, an increase in osteoprotegerin expression, and a decrease in serum tartrate-resistant acid phosphatase (TRAP5b) concentration. mBMPR1A treatment also increased bone mass and strength in mice with bone loss due to estrogen deficiency. In conclusion, mBMPR1A-mFc stimulates osteoblastic bone formation and decreases bone resorption, which leads to an increase in bone mass, and offers a promising unique alternative for the treatment of bone-related disorders.
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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.