ReviewBone2010
Control of RANKL gene expression.
Review in Bone, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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
92 citing papers in PubMed, 158 citations in OpenAlex.
- Osteocyte parvalbumin mediates mechanotransduction to attenuate osteoarthritis.Nature communications · 2026Article
- Hybrid extracellular vesicles for targeted delivery of therapeutic cargoes to combat osteoporotic bone loss.Cell biomaterials · 2026Article
- Severe Hypocalcemia During JAK1/2 Inhibitor Therapy for Myelofibrosis in a Patient with Liver Cirrhosis.Internal medicine (Tokyo, Japan) · 2025Article
- Role of Masticatory Force in Modulating Jawbone Immunity and Bone Homeostasis: A Review.International journal of molecular sciences · 2025Review
- Roles of osteoclasts in pathological conditions.Pathology international · 2025Review
- Critical signaling pathways in osteoclast differentiation and bone resorption: mechanisms and therapeutic implications for periprosthetic osteolysis.Frontiers in cell and developmental biology · 2025Review
- Building a modular and multi-cellular virtual twin of the synovial joint in Rheumatoid Arthritis.NPJ digital medicine · 2024Article
- MicroRNAs in fluorosis pathogenesis: impact on dental, skeletal, and soft tissues.Archives of toxicology · 2024Review
- Brown fat-specific mitoribosomal function is crucial for preventing cold exposure-induced bone loss.Cellular and molecular life sciences : CMLS · 2024Article
- The neutrophil-osteogenic cell axis promotes bone destruction in periodontitis.International journal of oral science · 2024Article
- Impact of deoxynivalenol in a calcium depletion and repletion nutritional strategy in piglets.Journal of animal science · 2024Article
- Osteoclasts at Bone Remodeling: Order from Order.Results and problems in cell differentiation · 2024Review
- The RANK-RANKL-OPG System: A Multifaceted Regulator of Homeostasis, Immunity, and Cancer.Medicina (Kaunas, Lithuania) · 2023Review
- Identification of an intronic enhancer regulating RANKL expression in osteocytic cells.Bone research · 2023Article
- Single-cell RNA sequencing reveals differential expression of EGFL7 and VEGF in giant-cell tumor of bone and osteosarcoma.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Osteocytes: Their Lacunocanalicular Structure and Mechanoresponses.International journal of molecular sciences · 2022Review
- Effect of vitamin D supplementation on OPG/RANKL signalling activities in endothelial tissue damage in diet-induced diabetic rat model.Pharmacological reports : PR · 2022Article
- Molecular Mechanisms Leading from Periodontal Disease to Cancer.International journal of molecular sciences · 2022Review
- Pathomechanisms of bone loss in rheumatoid arthritis.Frontiers in medicine · 2022Review
- Reconstruction and repair, using mini-plate and bone graft for persons living with HIV with giant cell tumor of long bone: retrospective analysis of a single-center experience.AIDS research and therapy · 2021Article
32 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
1 author at 1 institution in 1 country.
Funding
Abstract
Osteoclasts are highly specialized cells capable of degrading mineralized tissue and form at different regions of bone to meet different physiological needs, such as mobilization of calcium, modeling of bone structure, and remodeling of bone matrix. Osteoclast production is elevated in a number of pathological conditions, many of which lead to loss of bone mass. Whether normal or pathological, osteoclastogenesis strictly depends upon support from accessory cells which supply cytokines required for osteoclast differentiation. Only one of these cytokines, receptor activator of NFkappaB ligand (RANKL), is absolutely essential for osteoclast formation throughout life and is thus expressed by all cell types that support osteoclast differentiation. The central role of RANKL in bone resorption is highlighted by the fact that it is the basis for a new therapy to inhibit bone loss. This review will discuss mechanisms that control RANKL gene expression in different osteoclast-support cells and how the study of such mechanisms may lead to a better understanding of the cellular interactions that drive normal and pathological bone resorption.
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.