ArticleBiomaterials2015
Biotechnological approach for systemic delivery of membrane Receptor Activator of NF-κB Ligand (RANKL) active domain into the circulation.
Article in Biomaterials, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 25 citations in OpenAlex.
- Osteopetrosis: Pathogenesis, Clinical Management, and Emerging Therapies.Current osteoporosis reports · 2026Review
- High Bone Mass Disorders: New Insights From Connecting the Clinic and the Bench.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Review
- Circulating Extracellular Vesicles Express Receptor Activator of Nuclear Factor κB Ligand and Other Molecules Informative of the Bone Metabolic Status of Mouse Models of Experimentally Induced Osteoporosis.Calcified tissue international · 2023Article
- Identification of a binding site on soluble RANKL that can be targeted to inhibit soluble RANK-RANKL interactions and treat osteoporosis.Nature communications · 2022Article
- Identification of novel mutation in RANKL by whole-exome sequencing in a Thai family with osteopetrosis; a case report and review of RANKL osteopetrosis.Molecular genetics & genomic medicine · 2021Review
- Autosomal recessive osteopetrosis: mechanisms and treatments.Disease models & mechanisms · 2021Review
- The Charming World of the Extracellular Matrix: A Dynamic and Protective Network of the Intestinal Wall.Frontiers in medicine · 2021Review
- The Role of Extracellular Vesicles (EVs) in the Epigenetic Regulation of Bone Metabolism and Osteoporosis.International journal of molecular sciences · 2020Review
- New 8-Molecules (Basel, Switzerland) · 2020Article
- Osteoclast-derived apoptotic bodies show extended biological effects of parental cell in promoting bone defect healing.Theranostics · 2020Article
- Tumour-Derived Extracellular Vesicles (EVs): A Dangerous "Message in A Bottle" for Bone.International journal of molecular sciences · 2019Review
- One Disease, Many Genes: Implications for the Treatment of Osteopetroses.Frontiers in endocrinology · 2019Review
- Mesenchymal Stromal Cell-Seeded Biomimetic Scaffolds as a Factory of Soluble RANKL in Rankl-Deficient Osteopetrosis.Stem cells translational medicine · 2019Article
- MMP14 is a novel target of PTH signaling in osteocytes that controls resorption by regulating soluble RANKL production.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Silicon Nitride: A Synthetic Mineral for Vertebrate Biology.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Deficiency of Receptor Activator of NF-κB Ligand (RANKL) prevents osteoclast formation causing osteopetrosis. RANKL is a membrane-bound protein cleaved into active soluble (s)RANKL by metalloproteinase 14 (MMP14). We created a bio-device that harbors primary osteoblasts, cultured on 3D hydroxyapatite scaffolds carrying immobilized MMP14 catalytic domain. Scaffolds were sealed in diffusion chambers and implanted in RANKL-deficient mice. Mice received 1 or 2 diffusion chambers, once or twice and were sacrificed after 1 or 2 months from implants. A progressive increase of body weight was observed in the implanted groups. Histological sections of tibias of non-implanted mice were negative for the osteoclast marker Tartrate-Resistant Acid Phosphatase (TRAcP), consistent with the lack of osteoclasts. In contrast, tibias excised from implanted mice showed TRAcP-positive cells in the bone marrow and on the bone surface, these latter morphologically similar to mature osteoclasts. In mice implanted with 4 diffusion chambers total, we noted the highest number and size of TRAcP-positive cells, with quantifiable eroded bone surface and significant reduction of trabecular bone volume. These data demonstrate that our bio-device delivers effective sRANKL, inducing osteoclastogenesis in RANKL-deficient mice, supporting the feasibility of an innovative experimental strategy to treat systemic cytokine deficiencies.
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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.