ArticleCells2019
Bone Marrow Derived Extracellular Vesicles Activate Osteoclast Differentiation in Traumatic Brain Injury Induced Bone Loss.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.
What it found
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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
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.
- Beyond the initial impact: a systematic review of post-traumatic bone loss and its mechanisms.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Pooled it
- A systematic review and meta-analysis of factors involved in bone flap resorption after decompressive craniectomy.Neurosurgical review · 2022Pooled it
- Exosomes in bone health and disease: cellular crosstalk, systemic signaling, and AI-driven advances in regenerative therapy.Stem cell research & therapy · 2026Review
- Severe traumatic brain injury and risk for osteoporosis: a Mendelian randomization study.BMC medical genomics · 2025Article
- Bone-organ axes: bidirectional crosstalk.Military Medical Research · 2024Review
- Mechanism of Circ_HECW2 regulating osteoblast apoptosis in osteoporosis by attenuating the maturation of miR-1224-5p.Journal of orthopaedic surgery and research · 2024Article
- Unraveling the Emerging Niche Role of Extracellular Vesicles (EVs) in Traumatic Brain Injury (TBI).CNS & neurological disorders drug targets · 2024Review
- Role of exosomal ncRNAs in traumatic brain injury.Non-coding RNA research · 2023Review
- Bidirectional Communication Between the Brain and Other Organs: The Role of Extracellular Vesicles.Cellular and molecular neurobiology · 2023Review
- Bone marrow-derived exosomes promote inflammation and osteoclast differentiation in high-turnover renal osteodystrophy.Renal failure · 2023Article
- Clinically-driven design of novel methods of investigation on skeletal health status in neurological disorders. The case of the traumatic brain injuries.Frontiers in neurology · 2023Article
- Macromolecular Dexamethasone Prodrug Ameliorates Neuroinflammation and Prevents Bone Loss Associated with Traumatic Brain Injury.Molecular pharmaceutics · 2022Article
- Cell-Derived Exosomes as Therapeutic Strategies and Exosome-Derived microRNAs as Biomarkers for Traumatic Brain Injury.Journal of clinical medicine · 2022Review
- Article
- miRNA-92a-3p regulates osteoblast differentiation in patients with concomitant limb fractures and TBI via IBSP/PI3K-AKT inhibition.Molecular therapy. Nucleic acids · 2021Article
- Effect of exosomeZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021Article
- Germacrone alleviates neurological deficits following traumatic brain injury by modulating neuroinflammation and oxidative stress.BMC complementary medicine and therapies · 2021Article
- Early Reciprocal Effects in a Murine Model of Traumatic Brain Injury and Femoral Fracture.Mediators of inflammation · 2021Article
- Crosstalk of Brain and Bone-Clinical Observations and Their Molecular Bases.International journal of molecular sciences · 2020Review
- Effects of Neurological Disorders on Bone Health.Frontiers in psychology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a major source of worldwide morbidity and mortality. Patients suffering from TBI exhibit a higher susceptibility to bone loss and an increased rate of bone fractures; however, the underlying mechanisms remain poorly defined. Herein, we observed significantly lower bone quality and elevated levels of inflammation in bone and bone marrow niche after controlled cortical impact-induced TBI in in vivo CD-1 mice. Further, we identified dysregulated NF-κB signaling, an established mediator of osteoclast differentiation and bone loss, within the bone marrow niche of TBI mice. Ex vivo studies revealed increased osteoclast differentiation in bone marrow-derived cells from TBI mice, as compared to sham injured mice. We also found bone marrow derived extracellular vesicles (EVs) from TBI mice enhanced the colony forming ability and osteoclast differentiation efficacy and activated NF-κB signaling genes in bone marrow-derived cells. Additionally, we showed that miRNA-1224 up-regulated in bone marrow-derived EVs cargo of TBI. Taken together, we provide evidence that TBI-induced inflammatory stress on bone and the bone marrow niche may activate NF-κB leading to accelerated bone loss. Targeted inhibition of these signaling pathways may reverse TBI-induced bone loss and reduce fracture rates.
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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.