ArticleScience signaling2021
Augmented BMP signaling commits cranial neural crest cells to a chondrogenic fate by suppressing autophagic β-catenin degradation.
Article in Science signaling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- Neurogenic heterotopic ossification: from molecular mechanisms to clinical treatment.Journal of orthopaedic translation · 2026Review
- TGF-β/BMP signaling in skeletal biology: molecular mechanisms, regulatory networks, and therapeutic implications in development, regeneration, and disease.Bone research · 2026Review
- Article
- Nf2/FGFR1/AKT axis directs cranial neural crest-derived skull morphogenesis via collagen synthesis and trafficking.JCI insight · 2025Article
- PTHrP buffers Wnt/β-catenin activity through a PKC-ζ involved negative feedback loop to maintain articular cartilage homeostasis and attenuate osteoarthritis.Journal of orthopaedic translation · 2025Article
- Advancements in mechanisms and drug treatments for fibrodysplasia ossificans progressiva.Journal of Zhejiang University. Science. B · 2025Review
- Interplay between ALK2Cell death discovery · 2025Article
- The Critical Role of Autophagy in the Pathogenesis of Diabetic Osteoporosis: Mechanisms and Therapeutic Measures.Drug design, development and therapy · 2025Review
- SIRT1 and exercise-induced bone metabolism: a regulatory nexus.Frontiers in cell and developmental biology · 2025Review
- Modeling of skeletal development and diseases using human pluripotent stem cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Review
- A loss of primary cilia by a reduction in mTOR signaling correlates with age-related deteriorations in condylar cartilage.GeroScience · 2024Article
- The level of protein in the maternal murine diet modulates the facial appearance of the offspring via mTORC1 signaling.Nature communications · 2024Article
- Exploring the origins of neurodevelopmental proteasomopathies associated with cardiac malformations: are neural crest cells central to certain pathological mechanisms?Frontiers in cell and developmental biology · 2024Article
- [Oridonin suppresses the effect of thioacetamide for promoting osteoclast differentiation of RAW264.7 cells and inhibiting osteoblast differentiation of bone mesenchymal stem cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Article
- Review
- Neural crest cells and fetal alcohol spectrum disorders: Mechanisms and potential targets for prevention.Pharmacological research · 2023Review
- Oridonin Attenuates Thioacetamide-Induced Osteoclastogenesis Through MAPK/NF-κB Pathway and Thioacetamide-Inhibited Osteoblastogenesis Through BMP-2/RUNX2 Pathway.Calcified tissue international · 2023Article
- SMAD6 variants in nonsyndromic craniosynostosis.European journal of human genetics : EJHG · 2023Article
- Augmentation of BMP Signaling in Cranial Neural Crest Cells Leads to Premature Cranial Sutures Fusion through Endochondral Ossification in Mice.JBMR plus · 2023Article
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Cranial neural crest cells (CNCCs) are a population of multipotent stem cells that give rise to craniofacial bone and cartilage during development. Bone morphogenetic protein (BMP) signaling and autophagy have been individually implicated in stem cell homeostasis. Mutations that cause constitutive activation of the BMP type I receptor ACVR1 cause the congenital disorder fibrodysplasia ossificans progressiva (FOP), which is characterized by ectopic cartilage and bone in connective tissues in the trunk and sometimes includes ectopic craniofacial bones. Here, we showed that enhanced BMP signaling through the constitutively activated ACVR1 (ca-ACVR1) in CNCCs in mice induced ectopic cartilage formation in the craniofacial region through an autophagy-dependent mechanism. Enhanced BMP signaling suppressed autophagy by activating mTORC1, thus blocking the autophagic degradation of β-catenin, which, in turn, caused CNCCs to adopt a chondrogenic identity. Transient blockade of mTORC1, reactivation of autophagy, or suppression of Wnt-β-catenin signaling reduced ectopic cartilages in ca
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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.