ArticlePLoS biology2018
Differential aging of growth plate cartilage underlies differences in bone length and thus helps determine skeletal proportions.
Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 66 citations in OpenAlex.
- Aggrecan deficiency does not increase susceptibility to estrogen-induced growth plate senescence.Journal of the Endocrine Society · 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
- Alcohol consumption exacerbates high-fat diet-mediated disruptions in myelopoiesis and osteoclastogenesis in mouse models of metabolic dysfunction-associated liver diseases.Frontiers in endocrinology · 2026Article
- Emerging molecular mechanisms of the ECM-exosome growth-plate axis in idiopathic short stature.Frontiers in cell and developmental biology · 2026Review
- Cellular and genetic mechanisms that shape the development and evolution of tail vertebral proportion in mice and jerboas.Nature communications · 2025Article
- A Retinoid Antagonist Attenuates Bone Growth Inhibition Caused by Growth Plate Injury in Mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Growth plate closure and therapeutic interventions.Clinical and experimental pediatrics · 2024Article
- Article
- The Manganese-Bone Connection: Investigating the Role of Manganese in Bone Health.Journal of clinical medicine · 2024Review
- Microstructure changes and miRNA-mRNA network in a developmental dysplasia of the hip rat model.iScience · 2024Article
- Exercise promotes osteogenic differentiation by activating the long non-coding RNA H19/microRNA-149 axis.World journal of orthopedics · 2024Article
- Compensatory growth and recovery of cartilage cytoarchitecture after transient cell death in fetal mouse limbs.Nature communications · 2024Article
- N-cadherin and β1 integrin coordinately regulate growth plate cartilage architecture.Molecular biology of the cell · 2024Article
- Endothelial SMAD1/5 signaling couples angiogenesis to osteogenesis in juvenile bone.Communications biology · 2024Article
- Humero-femoral index and diabetes risk in the US population- a case study.Journal of diabetes and metabolic disorders · 2023Article
- Article
- Nutrient-regulated dynamics of chondroprogenitors in the postnatal murine growth plate.Bone research · 2023Article
- The genetic architecture of the human skeletal form.bioRxiv : the preprint server for biology · 2023Article
- Identification of novel genes includingFrontiers in endocrinology · 2023Article
- Periosteal stem cells control growth plate stem cells during postnatal skeletal growth.Nature communications · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Bones at different anatomical locations vary dramatically in size. For example, human femurs are 20-fold longer than the phalanges in the fingers and toes. The mechanisms responsible for these size differences are poorly understood. Bone elongation occurs at the growth plates and advances rapidly in early life but then progressively slows due to a developmental program termed "growth plate senescence." This developmental program includes declines in cell proliferation and hypertrophy, depletion of cells in all growth plate zones, and extensive underlying changes in the expression of growth-regulating genes. Here, we show evidence that these functional, structural, and molecular senescent changes occur earlier in the growth plates of smaller bones (metacarpals, phalanges) than in the growth plates of larger bones (femurs, tibias) and that this differential aging contributes to the disparities in bone length. We also show evidence that the molecular mechanisms that underlie the differential aging between different bones involve modulation of critical paracrine regulatory pathways, including insulin-like growth factor (Igf), bone morphogenetic protein (Bmp), and Wingless and Int-1 (Wnt) signaling. Taken together, the findings reveal that the striking disparities in the lengths of different bones, which characterize normal mammalian skeletal proportions, is achieved in part by modulating the progression of growth plate senescence.
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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.