ArticleMolecular endocrinology (Baltimore, Md.)2012
Reduced bone turnover in mice lacking the P2Y13 receptor of ADP.
Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Characterization of Potency of the P2Y13 Receptor Agonists: A Meta-Analysis.International journal of molecular sciences · 2021Pooled it
- Silencing P2YCell communication and signaling : CCS · 2025Article
- Application of Systematic Review and Meta-Analysis in Musculoskeletal Research.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Adenosine diphosphate released from stressed cells triggers mitochondrial transfer to achieve tissue homeostasis.PLoS biology · 2024Article
- P2Y13 receptor deficiency favors adipose tissue lipolysis and worsens insulin resistance and fatty liver disease.JCI insight · 2024Article
- InDel and CNV within theAnimals : an open access journal from MDPI · 2023Article
- Extracellular ATP and its derivatives provide spatiotemporal guidance for bone adaptation to wide spectrum of physical forces.Bone reports · 2022Review
- Mechanical Disturbance of Osteoclasts Induces ATP Release That Leads to Protein Synthesis in Skeletal Muscle through an Akt-mTOR Signaling Pathway.International journal of molecular sciences · 2022Article
- Identification of key biomarkers in steroid-induced osteonecrosis of the femoral head and their correlation with immune infiltration by bioinformatics analysis.BMC musculoskeletal disorders · 2022Article
- Absence of P2YFrontiers in endocrinology · 2022Article
- Review
- P2Y Receptors in Bone - Anabolic, Catabolic, or Both?Frontiers in endocrinology · 2021Review
- Role of UDP-Sugar Receptor P2YInternational journal of molecular sciences · 2020Article
- The role of GPCRs in bone diseases and dysfunctions.Bone research · 2019Review
- Small Molecules Enhance Scaffold-Based Bone Grafts via Purinergic Receptor Signaling in Stem Cells.International journal of molecular sciences · 2018Review
- P2X7 receptor regulates osteoclast function and bone loss in a mouse model of osteoporosis.Scientific reports · 2018Article
- Disruption of the Microglial ADP Receptor P2YFrontiers in cellular neuroscience · 2018Article
- P2YJournal of pain research · 2017Article
- Gs/Gi Regulation of Bone Cell Differentiation: Review and Insights from Engineered Receptors.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2016Review
- The frequency of osteolytic bone metastasis is determined by conditions of the soil, not the number of seeds; evidence from in vivo models of breast and prostate cancer.Journal of experimental & clinical cancer research : CR · 2015Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is a condition of excessive and uncoupled bone turnover, in which osteoclastic resorption exceeds osteoblastic bone formation, resulting in an overall net bone loss, bone fragility, and morbidity. Although numerous treatments have been developed to inhibit bone loss by blocking osteoclastic bone resorption, understanding of the mechanisms behind bone loss is incomplete. The purinergic signaling system is emerging to be a pivotal regulator of bone homeostasis, and extracellular ADP has previously been shown to be a powerful osteolytic agent in vitro. We report here that deletion of the P2Y(13) receptor, a G protein-coupled receptor for extracellular ADP, leads to a 40% reduction in trabecular bone mass, 50% reduction in osteoblast and osteoclast numbers in vivo, as well as activity in vitro, and an overall 50% reduction in the rate of bone remodeling in mice in vivo. Down-regulation of RhoA/ROCK I signaling and a reduced ratio of receptor activator of nuclear factor κB ligand/osteoprotegerin observed in osteoblasts from P2Y(13)R(-/-) mice might explain this bone phenotype. Furthermore, because one of the main causes of osteoporosis in older women is lack of estrogen, we examined the effect of ovariectomy of the P2Y(13)R(-/-) mice and found them to be protected from ovariectomy-induced bone loss by up to 65%. These data confirm a role of purinergic ADP signaling in the skeleton, whereby deletion of the P2Y(13) receptor leads to reduced bone turnover rates, which provide a protective advantage in conditions of accelerated bone turnover such as oestrogen deficiency-induced osteoporosis.
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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.