ArticleDevelopment (Cambridge, England)2009
BMP canonical Smad signaling through Smad1 and Smad5 is required for endochondral bone formation.
Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 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.
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Who cites it
198 citing papers in PubMed, 382 citations in OpenAlex.
- CK2.1 Activates Chondrogenesis by Regulation of the p38 Mitogen-Activated Protein Kinase Pathway.Kinases and phosphatases · 2026Article
- miR-433 targets BMP and Indian hedgehog signaling to coordinate murine postnatal growth plate dynamics.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- Heterotopic Ossification: Molecular Drivers, Subtype-Specific Mechanisms, and Translational Therapeutic Advances.Biomolecules · 2026Review
- Dichotomous SMAD2/3 regulation and selective antihypertrophic activity of heparin during in vitro chondrogenesis of mesenchymal stromal cells.Cellular & molecular biology letters · 2026Article
- Chondrogenic potential of mesenchymal progenitors from somatic and cartilage-derived iPSCs is predicted by their transcriptomic signatures.Genes & diseases · 2026Article
- A Heparin-Functionalized Scaffold with HB-EGF Immobilization for Tissue Engineering.Advanced healthcare materials · 2026Article
- CRISPR-mediated conditional mutagenesis ofbioRxiv : the preprint server for biology · 2026Article
- TGF-β/BMP signaling in skeletal biology: molecular mechanisms, regulatory networks, and therapeutic implications in development, regeneration, and disease.Bone research · 2026Review
- Innovative tissue engineering strategies for auricular regeneration in microtia: Current advances and future perspectives.Regenerative therapy · 2025Review
- Intra-Articular Delivery of Nanoemulsified Curcumin Ameliorates Joint Degeneration in a Chemically Induced Model of Osteoarthritis.International journal of molecular sciences · 2025Article
- Cranial base synostosis in mice caused by upregulation of Wnt following partial inhibition of Shh.BMC biology · 2025Article
- Genetics of morphological hip abnormalities and their implications for osteoarthritis: a scoping review.Journal of hip preservation surgery · 2025Review
- Molecular Determinants of Bone Plasticity Regeneration After Trauma: Forensic Consequences.International journal of molecular sciences · 2025Review
- BMP-2 generates a functional bone marrow niche by inducing the differentiation of local mesenchymal cells into CAR cells.Blood advances · 2025Article
- Distinct BMP-Smad signaling outputs confer diverse functions in dental mesenchyme.Development (Cambridge, England) · 2025Article
- TGF-β inhibitors: the future for prevention and treatment of liver fibrosis?Frontiers in immunology · 2025Review
- Metabolic reprogramming in skeletal cell differentiation.Bone research · 2024Review
- Regulation of Bone Morphogenetic Protein Receptor Type II Expression byInternational journal of molecular sciences · 2024Article
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138 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Bone morphogenetic protein (BMP) signaling is required for endochondral bone formation. However, whether or not the effects of BMPs are mediated via canonical Smad pathways or through noncanonical pathways is unknown. In this study we have determined the role of receptor Smads 1, 5 and 8 in chondrogenesis. Deletion of individual Smads results in viable and fertile mice. Combined loss of Smads 1, 5 and 8, however, results in severe chondrodysplasia. Smad1/5(CKO) (cartilage-specific knockout) mutant mice are nearly identical to Smad1/5(CKO);Smad8(-/-) mutants, indicating that Smads 1 and 5 have overlapping functions and are more important than Smad8 in cartilage. The Smad1/5(CKO) phenotype is more severe than that of Smad4(CKO) mice, challenging the dogma, at least in chondrocytes, that Smad4 is required to mediate Smad signaling through BMP pathways. The chondrodysplasia in Smad1/5(CKO) mice is accompanied by imbalances in cross-talk between the BMP, FGF and Ihh/PTHrP pathways. We show that Ihh is a direct target of BMP pathways in chondrocytes, and that FGF exerts antagonistic effects on Ihh expression. Finally, we tested whether FGF exerts its antagonistic effects directly through Smad linker phosphorylation. The results support the alternative conclusion that the effects of FGFs on BMP signaling are indirect in vivo.
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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.