ArticleAutophagy2015
FGFR3/fibroblast growth factor receptor 3 inhibits autophagy through decreasing the ATG12-ATG5 conjugate, leading to the delay of cartilage development in achondroplasia.
Article in Autophagy, 2015. 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, 86 citations in OpenAlex.
- Biomimetic ECM collagen hydrogel induces chondrogenic differentiation of BMSCs by activating autophagy through POU5F1-mediated AMPK/mTOR signaling pathway.Theranostics · 2026Article
- Advances in the mechanism and therapies of achondroplasia.Genes & diseases · 2025Review
- Fibroblast growth factor receptor 3 mutation promotes HSPB6-mediated cuproptosis in hypochondroplasia by impairing chondrocyte autophagy.Journal of orthopaedic translation · 2025Article
- FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia.Bone research · 2025Article
- Il-1β Promotes Superficial Zone Cells Senescence in Articular Cartilage by Inhibiting Autophagy.Cartilage · 2024Article
- FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies.Cancer communications (London, England) · 2024Review
- FGFR2-triggered autophagy and activation of Nrf-2 reduce breast cancer cell response to anti-ER drugs.Cellular & molecular biology letters · 2024Article
- Secukinumab plays a synergistic role with starvation therapy in promoting autophagic cell death of hepatocellular carcinoma via inhibiting IL-17A-increased BCL2 level.In vitro cellular & developmental biology. Animal · 2023Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Between Inflammation and Autophagy: The Role of Leptin-Adiponectin Axis in Cardiac Remodeling.Journal of inflammation research · 2021Review
- Gold Nanomaterials and Bone/Cartilage Tissue Engineering: Biomedical Applications and Molecular Mechanisms.Frontiers in chemistry · 2021Review
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Progress of orthopaedic research in China over the last decade.Journal of orthopaedic translation · 2020Article
- Oestrogen-activated autophagy has a negative effect on the anti-osteoclastogenic function of oestrogen.Cell proliferation · 2020Article
- Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1BioMed research international · 2020Article
- Article
- Puerarin inhibits the osteoclastogenesis by inhibiting RANKL-dependent and -independent autophagic responses.BMC complementary and alternative medicine · 2019Article
- The Aberrant Expression of the Mesenchymal Variant of FGFR2 in the Epithelial Context Inhibits Autophagy.Cells · 2019Article
- miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7.Scientific reports · 2019Article
- Water Extract of Sporoderm-Broken Spores ofOncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FGFR3 (fibroblast growth factor receptor 3) is a negative regulator of endochondral ossification. Gain-of-function mutations in FGFR3 are responsible for achondroplasia, the most common genetic form of dwarfism in humans. Autophagy, an evolutionarily conserved catabolic process, maintains chondrocyte viability in the growth plate under stress conditions, such as hypoxia and nutritional deficiencies. However, the role of autophagy and its underlying molecular mechanisms in achondroplasia remain elusive. In this study, we found activated FGFR3 signaling inhibited autophagic activity in chondrocytes, both in vivo and in vitro. By employing an embryonic bone culture system, we demonstrated that treatment with autophagy inhibitor 3-MA or chloroquine led to cartilage growth retardation, which mimics the effect of activated-FGFR3 signaling on chondrogenesis. Furthermore, we found that FGFR3 interacted with ATG12-ATG5 conjugate by binding to ATG5. More intriguingly, FGFR3 signaling was found to decrease the protein level of ATG12-ATG5 conjugate. Consistently, using in vitro chondrogenic differentiation assay system, we showed that the ATG12-ATG5 conjugate was essential for the viability and differentiation of chondrocytes. Transient transfection of ATG5 partially rescued FGFR3-mediated inhibition on chondrocyte viability and differentiation. Our findings reveal that FGFR3 inhibits the autophagic activity by decreasing the ATG12-ATG5 conjugate level, which may play an essential role in the pathogenesis of achondroplasia.
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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.