ArticlePeerJ2021
Zoledronic acid promotes osteoclasts ferroptosis by inhibiting FBXO9-mediated p53 ubiquitination and degradation.
Article in PeerJ, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- The role of ferroptosis in osteoporosis: a cellular perspective on osteoblast, osteoclast and osteocyte dysfunction.Frontiers in endocrinology · 2026Pooled it
- Targeting Ferroptosis With Natural Products for the Treatment of Skeletal System Disease: An Updated Review.Journal of cellular and molecular medicine · 2026Review
- Spectrum and functions of ion channels and transporters in osteoclasts.Bone research · 2026Review
- Ferroptosis in compromised bone healing after trauma: from the iron/ROS microenvironment to non-union and bone defect reconstruction.Frontiers in medicine · 2026Review
- Ferroptosis in osteoporosis: core mechanisms, cell-specific effects in bone remodelling, and therapeutic perspectives.Frontiers in endocrinology · 2026Review
- Zingerone treats postmenopausal osteoporosis via increased ferroptosis sensitivity by p53-mediated regulation of SAT1 and GPX4 expression.Communications biology · 2025Article
- The role of ferroptosis in osteoporosis: from pathogenic mechanisms to natural product-driven therapeutic innovations.Frontiers in medicine · 2025Review
- Matrine in cancer therapy: antitumor mechanisms and nano-delivery strategies.Frontiers in pharmacology · 2025Review
- Ferroptosis at the intersection of osteoarthritis and bone metabolism: mechanistic links and therapeutic prospects.Frontiers in cell and developmental biology · 2025Review
- The Potential Regulatory Role of Ferroptosis in Orthodontically Induced Inflammatory Root Resorption.International journal of molecular sciences · 2024Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Repair and regeneration: ferroptosis in the process of remodeling and fibrosis in impaired organs.Cell death discovery · 2024Review
- Targeting nanoplatform synergistic glutathione depletion-enhanced chemodynamic, microwave dynamic, and selective-microwave thermal to treat lung cancer bone metastasis.Bioactive materials · 2024Article
- An update on the role of ferroptosis in the pathogenesis of osteoporosis.EFORT open reviews · 2024Review
- Type 2 diabetic mellitus related osteoporosis: focusing on ferroptosis.Journal of translational medicine · 2024Review
- Mechanism and application prospect of ferroptosis inhibitors in improving osteoporosis.Frontiers in endocrinology · 2024Review
- Decoding ferroptosis: transforming orthopedic disease management.Frontiers in pharmacology · 2024Review
- Review
- Prevention and treatment of osteoporosis with natural products: Regulatory mechanism based on cell ferroptosis.Journal of orthopaedic surgery and research · 2023Review
- The Potential Roles of Ferroptosis in Pathophysiology and Treatment of Musculoskeletal Diseases-Opportunities, Challenges, and Perspectives.Journal of clinical medicine · 2023Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bisphosphonates (BPs)-related osteonecrosis of jaw (BRONJ) is a severe complication of the long-term administration of BPs. The development of BRONJ is associated with the cell death of osteoclasts, but the underlying mechanism remains unclear. In the current study, the role of Zoledronic acid (ZA), a kind of bisphosphonates, in suppressing the growth of osteoclasts was investigated and its underlying mechanism was explored. The role of ZA in regulating osteoclasts function was evaluated in the RANKL-induced cell model. Cell viability was assessed by cell counting kit-8 (CCK-8) assay and fluorescein diacetate (FDA)-staining. We confirmed that ZA treatment suppressed cell viability of osteoclasts. Furthermore, ZA treatment led to osteoclasts death by facilitating osteoclasts ferroptosis, as evidenced by increased Fe
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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.