ArticleJournal of cellular biochemistry2011
Zoledronic acid inhibits macrophage SOCS3 expression and enhances cytokine production.
Article in Journal of cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 38 citations in OpenAlex.
- NLRP3 Activation With Bisphosphonate Use and the Risk of Incident Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2025Article
- Role of the suppressor of cytokine signaling-3 in the pathogenesis of Graves' orbitopathy.Frontiers in endocrinology · 2025Article
- Medication-related osteonecrosis of the jaw (MRONJ): a review of pathogenesis hypothesis and therapy strategies.Archives of toxicology · 2024Review
- Longitudinal single cell atlas identifies complex temporal relationship between type I interferon response and COVID-19 severity.Nature communications · 2024Article
- Prediction of musculoskeletal pain after the first intravenous zoledronic acid injection in patients with primary osteoporosis: development and evaluation of a new nomogram.BMC musculoskeletal disorders · 2023Article
- Interleukin-17 plays a role in dental pulp inflammation mediated by zoledronic acid: a mechanism unrelated to the Th17 immune response?Journal of applied oral science : revista FOB · 2023Article
- Predicting the acute-phase response fever risk in bisphosphonate-naive osteoporotic patients receiving their first dose of zoledronate.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2022Article
- Mechanisms of reduced leptin-mediated satiety signaling during obesity.International journal of obesity (2005) · 2022Article
- The Suppressor of Cytokine Signalling family of proteins and their potential impact on COVID-19 disease progression.Reviews in medical virology · 2022Review
- Macrophage Involvement in Medication-Related Osteonecrosis of the Jaw (MRONJ): A Comprehensive, Short Review.Cancers · 2022Review
- Association between vitamin D and zoledronate-induced acute-phase response fever risk in osteoporotic patients.Frontiers in endocrinology · 2022Article
- Compressive force strengthened the pro-inflammatory effect of zoledronic acid on il-1ß stimulated human periodontal fibroblasts.Clinical oral investigations · 2021Article
- IL-17 constrains natural killer cell activity by restraining IL-15-driven cell maturation via SOCS3.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Pathogenesis of medication-related osteonecrosis of the jaw: a comparative study of in vivo and in vitro trials.The Journal of international medical research · 2018Review
- Zoledronic acid exacerbates inflammation through M1 macrophage polarization.Inflammation and regeneration · 2018Article
- Multicenter Study on Observation of Acute-phase Responses After Infusion of Zoledronic Acid 5 mg in Chinese Women with Postmenopausal Osteoporosis.Orthopaedic surgery · 2017Observational
- An intrapleural administration of zoledronic acid for inoperable malignant mesothelioma patients: a phase I clinical study protocol.SpringerPlus · 2016Article
- Bisphosphonate Induces Osteonecrosis of the Jaw in Diabetic Mice via NLRP3/Caspase-1-Dependent IL-1β Mechanism.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
- SOCS Proteins in Macrophage Polarization and Function.Frontiers in immunology · 2014Review
- IL-17-mediated M1/M2 macrophage alteration contributes to pathogenesis of bisphosphonate-related osteonecrosis of the jaws.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Suppressor of cytokine signaling-3 (SOCS3) has multiple functions including inhibition of Janus kinase (Jak) activity, regulation of protein degradation, and suppression of cytokine signaling. SOCS3 modulates macrophage response to cytokines such as IL-6 and leptin that are systemically induced in obesity. Obesity is a suspected risk factor for SOCS3-related pathology such as rheumatoid arthritis and Crohn's disease as well as zoledronic acid (ZA)-induced osteonecrosis of the jaw (ONJ). Thus, understanding the ability of bisphosphonates to modulate SOCS3 is necessary to qualify their contribution to these disorders. ONJ occurs in up to 10% of patients using intravenous bisphosphonates and has an unknown pathogenesis that may be linked to decreased bone turnover, altered vascularity, bacterial invasion, and compromised wound healing. Given the increased risk of ONJ with obesity and importance of macrophages in wound healing, we hypothesized that amino-bisphosphonates could contribute to the pathogenesis of ONJ by regulating macrophage responses to cytokines such as leptin and IL-6. We report that ZA is a novel inhibitor of SOCS3 in primary macrophages and human ONJ biopsy specimens. Inhibition of SOCS3 by ZA resulted in significant increases in IL-6 production. SOCS3 transcription is regulated by nuclear accumulation of phosphorylated-Stat3 (P-Stat3). We found that ZA decreased phosphorylation of Stat3 in a mevalonate-pathway dependent manner. However, restoration of P-Stat3 was not sufficient to correct SOCS3 inhibition. We propose that disruption of macrophage SOCS3 expression by amino-bisphosphonates such as ZA may be a novel contributor to inflammatory phenotypes in obesity and the pathogenesis of ONJ.
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.