ReviewJBMR plus2018
Parathyroid Hormone Signaling in Osteocytes.
Review in JBMR plus, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
- Bone-Targeted Therapies and Spinal Morphometry in Postmenopausal Osteoporosis: A Real-World Longitudinal Retrospective Study.Bioengineering (Basel, Switzerland) · 2026Article
- Regulation of cAMP levels in osteocytes by mechano-sensitive focal adhesion kinase and phosphodiesterase 8A.iScience · 2026Article
- Proteoglycan Dynamics and Bone Quality: Molecular Regulation to Age-Related Fragility.Biomolecules · 2026Review
- Bone metabolism in primary hyperparathyroidism.Wiener klinische Wochenschrift · 2026Review
- Upregulation of Parathyroid Hormone Receptor 1 (International journal of molecular sciences · 2026Article
- Development of a severe rat refeeding syndrome model and mathematical modeling of the associated hypophosphatemia.NPJ systems biology and applications · 2026Article
- Developmental Pathways of Immature CD11cInternational journal of molecular sciences · 2026Review
- Jansen's Disease: Bone Abnormalities Beyond Chondrodysplasia.The Journal of clinical endocrinology and metabolism · 2025Article
- PTH counteracts Hippo signaling via Src-dependent YAP stabilization to enhance bone marrow stromal cell differentiation.JCI insight · 2025Article
- Differential bone and vessel type formation at superior and dura periosteum during cranial bone defect repair.Bone research · 2025Article
- Bone Disease in Primary Hyperparathyroidism-Changes Occurring in Bone Metabolism and New Potential Treatment Strategies.International journal of molecular sciences · 2024Review
- Review
- Etiological Mechanisms and Genetic/Biological Modulation Related to PTH1R in Primary Failure of Tooth Eruption.Calcified tissue international · 2024Review
- Inhibition of RANKL improves the skeletal phenotype of adenine-induced chronic kidney disease in mice.JBMR plus · 2024Article
- The osteocytic actions of glucocorticoids on bone mass, mechanical properties, or perilacunar remodeling outcomes are not rescued by PTH(1-34).Frontiers in endocrinology · 2024Article
- The role of magnesium in the pathogenesis of osteoporosis.Frontiers in endocrinology · 2024Review
- Comparative study in estrogen-depleted mice identifies skeletal and osteocyte transcriptomic responses to abaloparatide and teriparatide.JCI insight · 2023Article
- Determinants of Low Bone Turnover in Type 2 Diabetes-the Role of PTH.Calcified tissue international · 2022Observational
- The origins and roles of osteoclasts in bone development, homeostasis and repair.Development (Cambridge, England) · 2022Review
- NACA and LRP6 Are Part of a Common Genetic Pathway Necessary for Full Anabolic Response to Intermittent PTH.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteocytes are the most abundant cell type in bone and play a central role in orchestrating skeletal remodeling, in part by producing paracrine-acting factors that in turn influence osteoblast and osteoclast activity. Recent evidence has indicated that osteocytes are crucial cellular targets of parathyroid hormone (PTH). Here, we will review the cellular and molecular mechanisms through which PTH influences osteocyte function. Two well-studied PTH target genes in osteocytes are SOST and receptor activator of NF-κB ligand (RANKL). The molecular mechanisms through which PTH regulates expression of these two crucial target genes will be discussed. Beyond SOST and RANKL, PTH/PTH-related peptide (PTHrP) signaling in osteocytes may directly influence the way osteocytes remodel their perilacunar environment to influence bone homeostasis in a cell-autonomous manner. Here, I will highlight novel, additional mechanisms used by PTH and PTHrP to modulate bone homeostasis through effects in osteocytes. © 2017 The Authors.
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What OpenQuestion 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 OpenQuestion graph.