ArticleBone2020
Loss of BMP signaling mediated by BMPR1A in osteoblasts leads to differential bone phenotypes in mice depending on anatomical location of the bones.
Article in Bone, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
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
12 citing papers in PubMed, 23 citations in OpenAlex.
- Regional diversity of cranial skeletal stem cells governs bone morphogenetic protein-2 mediated bone regeneration.Nature communications · 2026Article
- Unexpected Promotion of Bone Regeneration by Inhibition of BMPR1A-Mediated BMP Signalling.Cell proliferation · 2026Article
- Role of lactoferrin in osteopenia and osteoporosis.Frontiers in nutrition · 2025Review
- Influence of bone morphogenetic protein (BMP) signaling and masticatory load on morphological alterations of the mouse mandible during postnatal development.Archives of oral biology · 2025Article
- EndoCompass Project: Research Roadmap for Calcium and Bone Endocrinology.Hormone research in paediatrics · 2025Review
- Family-based whole-exome sequencing implicates a variant in lysyl oxidase like 4 in atypical femur fractures.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Article
- The roles and regulatory mechanisms of TGF-β and BMP signaling in bone and cartilage development, homeostasis and disease.Cell research · 2024Review
- Activin receptor-like kinase 3: a critical modulator of development and function of mineralized tissues.Frontiers in cell and developmental biology · 2023Review
- Article
- Acvr1 deletion in osteoblasts impaired mandibular bone mass through compromised osteoblast differentiation and enhanced sRANKL-induced osteoclastogenesis.Journal of cellular physiology · 2021Article
- The Regulation of Growth in Developing, Homeostatic, and Regenerating Tetrapod Limbs: A Minireview.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 3 countries.
Funding
Abstract
Bone morphogenetic protein (BMP) signaling in osteoblasts plays critical roles in skeletal development and bone homeostasis. Our previous studies showed loss of function of BMPR1A, one of the type 1 receptors for BMPs, in osteoblasts results in increased trabecular bone mass in long bones due to an imbalance between bone formation and bone resorption. Decreased bone resorption was associated with an increased mature-to-immature collagen cross-link ratio and mineral-matrix ratios in the trabecular compartments, and increased tissue-level biomechanical properties. Here, we investigated the bone mass, bone composition and biomechanical properties of ribs and spines in the same genetically altered mouse line to compare outcomes by loss of BMPR1A functions in bones from different anatomic sites and developmental origins. Bone mass was significantly increased in both cortical and trabecular compartments of ribs with minimal to modest changes in compositions. While tissue-levels of biomechanical properties were not changed between control and mutant animals, whole bone levels of biomechanical properties were significantly increased in association with increased bone mass in the mutant ribs. For spines, mutant bones showed increased bone mass in both cortical and trabecular compartments with an increase of mineral content. These results emphasize the differential role of BMP signaling in osteoblasts in bones depending on their anatomical locations, functional loading requirements and developmental origin.
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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.