SynthesisFrontiers in endocrinology2026
The role of ferroptosis in osteoporosis: a cellular perspective on osteoblast, osteoclast and osteocyte dysfunction.
Synthesis in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Macrophage metabolic reprogramming via HIF-1α-glycolysis drives osteoblast ferroptosis and bone loss through an IL-6-STAT3-dependent redox axis.Redox report : communications in free radical research · 2026Article
- Oxidized-Lipid Signaling and Ferroptosis as Downstream Mechanisms of Titanium-Associated Peri-Implant Bone Loss.Antioxidants (Basel, Switzerland) · 2026Review
- Insights into taurine therapy for periodontitis: Targeting osteocyte ferroptosis to mitigate obesity-exacerbated bone damage.Redox biology · 2026Article
- Association of prognostic nutritional index with fecal incontinence and fecal incontinence severity index in individuals with osteoporosis: mediating roles of C-reactive protein and gamma-glutamyl transferase.Frontiers in nutrition · 2026Article
- Bone Marrow Immunometabolic Remodeling in Osteoporosis: From Systemic Risk Factors to Precision Intervention.International journal of general medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is characterized by an imbalance between bone resorption and bone formation, leading to the loss of both trabecular and cortical bone mass, ultimately resulting in an increased risk of fractures. Osteoporosis represents a major global health burden, predominantly affecting elderly individuals and postmenopausal women. With the continued growth of the aging population, the prevalence of osteoporosis is expected to increase, highlighting the urgent need for more effective therapeutic strategies. Ferroptosis, a recently characterized form of iron-dependent, non-apoptotic cell death, has emerged as an important mechanism contributing to the pathogenesis of osteoporosis. A better understanding of ferroptosis may therefore provide new insights into therapeutic development. This review summarizes current evidence regarding the role of ferroptosis in osteoporosis, with particular focus on its effects on osteoblasts, osteoclasts, and osteocytes, as well as the impact of aging, estrogen deficiency, diabetes, glucocorticoid exposure, and obesity on ferroptosis in osteogenic cells.
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.