ArticleBone2014
Osteocyte apoptosis is required for production of osteoclastogenic signals following bone fatigue in vivo.
Article in Bone, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- Reprogramming bone homeostasis: The recoupling-oriented framework of bidirectional regulation strategies for osteoporosis.iScience · 2026Review
- Metabolic disorders and osteoarthritis: novel insights into pathological mechanisms and therapeutic strategies.Life medicine · 2026Review
- Critical Overview of Molecular Insights into Osteoarthritis and Therapeutic Targets: Cytokines, RANKL, MMPs, Adipokines and Phosphate Dysregulation.International journal of molecular sciences · 2026Review
- Branched‑chain amino acid metabolism and bone metabolism: Implications for osteoporosis pathogenesis and therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- The paradigm-shifting roles of caspase-3 in cancer: from death towards resuscitation.Cancer cell international · 2026Review
- Cortical bone porosity is spatially heterogeneous and VEGF dependent in male bone.Disease models & mechanisms · 2026Article
- Effects of Thermal Environment on Bone Microenvironment: A Narrative Review.International journal of molecular sciences · 2025Review
- [Pathology of Cartilage-to-Bone Crosstalk: A New Angle for Animal Experimental Studies on Osteoarthritis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Review
- RANKL-mediated osteoclastic subchondral bone loss at a very early stage precedes subsequent cartilage degeneration and uncoupled bone remodeling in a mouse knee osteoarthritis model.Journal of orthopaedic surgery and research · 2025Article
- Novel aspects of biochemical assessment of bone remodeling and mineralization.Frontiers in endocrinology · 2025Review
- Article
- Pyroptosis in Skeleton Diseases: A Potential Therapeutic Target Based on Inflammatory Cell Death.International journal of molecular sciences · 2024Review
- Roles of Sp7 in osteoblasts for the proliferation, differentiation, and osteocyte process formation.Journal of orthopaedic translation · 2024Article
- Article
- Pannexins in the musculoskeletal system: new targets for development and disease progression.Bone research · 2024Review
- Article
- Early protection against bone stress injuries by mobilization of endogenous targeted bone remodeling.iScience · 2023Article
- Caspase-3 in glioma indicates an unfavorable prognosis by involving surrounding angiogenesis and tumor cell repopulation.Journal of neuro-oncology · 2023Article
- Mapping the Response of Human Osteocytes in Native Matrix to Mechanical Loading Using RNA Sequencing.JBMR plus · 2023Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Osteocyte apoptosis is spatially, temporally and functionally linked to the removal and replacement of microdamage in the bone. Recently we showed that microdamage elicits distinct responses in two populations of osteocytes near the injury site. Osteocytes directly adjacent to microdamage undergo apoptosis, whereas there is a second group of osteocytes located adjacent to the apoptotic population that upregulate expression of osteoclastogenic signaling molecules. In this study we used the pan-caspase inhibitor QVD to test the hypothesis that osteocyte apoptosis is an obligatory step in the production of key osteoclastogenic signals by in situ osteocytes in fatigue-damaged bone. We found, based on real-time PCR and immunohistochemistry assays, that expression of the apoptosis marker caspase-3 as well osteoclastogenic proteins RANKL and VEGF were increased following fatigue, while expression of the RANKL antagonist OPG decreased. However, when apoptosis was inhibited using QVD, these changes in gene expression were completely blocked. This dependence on apoptosis for neighboring non-apoptotic cells to produce signals that promote tissue remodeling also occurs in response to focal ischemic injury in the brain and heart, indicating that osteoclastic bone remodeling follows a common paradigm for localized tissue repair.
Indexed as
Identifiers
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.