ArticleCell proliferation2020
IGFBP7 acts as a negative regulator of RANKL-induced osteoclastogenesis and oestrogen deficiency-induced bone loss.
Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Systematic review of exosomes derived from various stem cell sources: function and therapeutic potential in disease modulation.Molecular biology reports · 2025Pooled it
- A Functional Shift of IGFBP3 in Osteoarthritis: From Cartilage Protection to Disease Promotion.Journal of inflammation research · 2026Review
- Tracing the pathways: how inflammatory cytokines and blood metabolites drive intervertebral disc degeneration.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2025Article
- IGFBP7 inhibition relieves LPS induced nucleus pulposus cell injury by regulating the ERK1/2 pathway.Cytotechnology · 2025Article
- Delayed Administration of IGFBP7 Improved Bone Defect Healing via ZO-1 Dependent Vessel Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Selection of the Anti-Osteoporosis Active Ingredients of Fructus Psoraleae-Eucommia-Drynariae Rhizoma Based on Solid-Phase Bio-Cell Chromatography and HPLC-MS Analysis.Food science & nutrition · 2025Article
- Conditioned Medium From Stem Cells of Human Exfoliated Deciduous Teeth Alleviates Mouse Osteoarthritis by Inducing sFRP1-Expressing M2 Macrophages.Stem cells translational medicine · 2024Article
- CD_99 G1 neutrophils modulate osteogenic differentiation of mesenchymal stem cells in the pathological process of ankylosing spondylitis.Annals of the rheumatic diseases · 2024Article
- CircDENND2D Inhibits PD-L1-Mediated Non-Small Cell Lung Cancer Metastasis and Immune Escape by Regulating miR-130b-3p/STK11 Axis.Biochemical genetics · 2023Article
- The Secretome of Parental and Bone Metastatic Breast Cancer Elicits Distinct Effects in Human Osteoclast Activity after Activation of β2 Adrenergic Signaling.Biomolecules · 2023Article
- Reversing the imbalance in bone homeostasis via sustained release of SIRT-1 agonist to promote bone healing under osteoporotic condition.Bioactive materials · 2023Article
- Parkin Inhibits RANKL-Induced Osteoclastogenesis and Ovariectomy-Induced Bone Loss.Biomolecules · 2022Article
- Skeletal disorders associated with the growth hormone-insulin-like growth factor 1 axis.Nature reviews. Endocrinology · 2022Review
- Therapeutic Treatments for Osteoporosis-Which Combination of Pills Is the Best among the Bad?International journal of molecular sciences · 2022Review
- Bioinformatics Analysis of the Key Genes and Pathways in Multiple Myeloma.International journal of general medicine · 2022Article
- The soluble CD83 protein prevents bone destruction by inhibiting the formation of osteoclasts and inducing resolution of inflammation in arthritis.Frontiers in immunology · 2022Article
- Evaluating Osteogenic Differentiation of Osteoblastic Precursors Upon Intermittent Administration of PTH/IGFBP7.Frontiers in pharmacology · 2022Article
- Excavating bioactivities of nanozyme to remodel microenvironment for protecting chondrocytes and delaying osteoarthritis.Bioactive materials · 2021Article
- Current knowledge on the genetic background of developmental dysplasia of the hip and the histomorphological status of the cartilage.Croatian medical journal · 2020Review
- IGFBP7 acts as a negative regulator of RANKL-induced osteoclastogenesis and oestrogen deficiency-induced bone loss.Cell proliferation · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesInsulin-like growth factor-binding protein 7 (IGFBP7) is a low-affinity insulin growth factor (IGF) binder that may play an important role in bone metabolism. We previously reported that IGFBP7 enhanced osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) via the Wnt/β-catenin signalling pathway. In this study, we tried to reveal its function in osteoclast differentiation and osteoporosis.
methodsWe used both in vitro and in vivo studies to investigate the effects of IGFBP7 on RANKL-induced osteoclastogenesis and osteoporosis, together with the underlying molecular mechanisms of these processes.
resultsWe show that IGFBP7 inhibited receptor activation of nuclear factor-κB (NF-κB) ligand (RANKL)-induced osteoclastogenesis, F-actin ring formation and bone resorption, which was confirmed by using recombinant IGFBP7 protein, lentivirus and siRNA. The NF-κB signalling pathway was inhibited during this process. Moreover, in a mouse ovariectomy-induced osteoporosis model, IGFBP7 treatment attenuated osteoporotic bone loss by inhibiting osteoclast activity.
conclusionsTaken together, these findings show that IGFBP7 suppressed osteoclastogenesis in vitro and in vivo and suggest that IGFBP7 is a negative regulator of osteoclastogenesis and plays a protective role in osteoporosis. These novel insights into IGFBP7 may facilitate the development of potential treatment strategies for oestrogen deficiency-induced osteoporosis and other osteoclast-related disorders.
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.