ArticleBone & joint research2025
G-protein-coupled estrogen receptor-1 facilitates chondrocyte proliferation in pubertal epiphyseal growth plate via PTHrP/Ihh regulation.
Article in Bone & joint research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- The regulatory significance of chondrocyte hypertrophy in maintaining chondrocyte homeostasis, regeneration and repair.Future science OA · 2026Review
- Coronal Plane Alignment of the Knee (CPAK) in children and adolescents : an analysis of 655 knees according to the CPAK classification.Bone & joint open · 2026Article
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- Sex-specific hormonal rescue of bone growth in PAPPA2-deficient mice : a role for cannabinoid receptors and STAT3.Bone & joint research · 2026Article
- GPER agonist G1 suppresses neuronal apoptosis mediated by endoplasmic reticulum stress after exertional heat stroke injury.Scientific reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Aims: Oestrogen drives long-bone development through various oestrogen receptors. G-protein-coupled oestrogen receptor-1 (GPER-1), a membrane oestrogen receptor, mediates longitudinal bone growth during early puberty; however, the underlying mechanisms remain unclear. Therefore, this study elucidated the mechanisms underlying GPER-1-mediated bone growth. Methods: A GPER-1 agonist (G1), GPER-1 antagonist (G15), and chondrocyte-specific GPER-1 knockout experiment ( Results: G1 treatment-induced GPER-1 activation increased tibial growth plate thickness, proliferative zone thickness, and chondrocyte proliferation in mice. The hypertrophic zone thickness and type X collagen-stained area decreased in four-week-old G1-treated mice compared with the control group. GPER-1 activation increased the PTHrP/Ihh ratio in the growth plates of four- and eight-week-old mice. In contrast, blocking or deleting GPER-1 decreased the proliferative zones of the growth plate, proliferative chondrocytes, and PTHrP/Ihh. Additionally, the hyperopic zones of the growth plates increased with GPER-1 deficiency. In vitro micromass-3D cultured chondrocyte studies confirmed that G1 treatment increased proliferation, decreased hypertrophy, and increased PTHrP/Ihh protein levels. Conclusion: This study demonstrates that GPER-1 maintains proliferation but suppresses chondrocyte hypertrophy in growth plates by upregulating PTHrP/Ihh during early puberty in male and female mice. Our findings suggest that GPER-1 may serve as a potential target for therapeutic modulation of linear bone growth during puberty.
Identifiers
What Socratic holds
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 Socratic graph.