ArticleNature communications2019
Increased autophagy in EphrinB2-deficient osteocytes is associated with elevated secondary mineralization and brittle bone.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Insights into the mechanism of vascular endothelial cells on bone biology.Bioscience reports · 2021Pooled it
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- Descendants of hypertrophic chondrocytes promote angiogenesis by secreting THBS4 during bone growth and injury repair.Bone research · 2025Article
- Differentiation of typical features between Fungal spondylitis and Brucellar spondylitis on CT and new applications of CT values in diagnosis of spinal infections.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2025Article
- Stress-induced fetal programming contributes to the manifestation of Duchenne muscular dystrophy iniScience · 2025Article
- Isolation, Purification, Generation, and Culture of Osteocytes.Methods in molecular biology (Clifton, N.J.) · 2025Article
- A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer.Journal of extracellular vesicles · 2024Article
- Osteoclast-derived coupling factors: origins and state-of-play Louis V Avioli lecture, ASBMR 2023.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- EphrinB2-mediated chondrocyte autophagy induces post-traumatic arthritis via rupture of cartilage homeostasis.Journal of cellular and molecular medicine · 2024Article
- Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone.Endocrine reviews · 2024Review
- Cell signaling and transcriptional regulation of osteoblast lineage commitment, differentiation, bone formation, and homeostasis.Cell discovery · 2024Review
- Autophagy, a double-edged sword for oral tissue regeneration.Journal of advanced research · 2024Review
- Exploring the Osteogenic Potential of Zinc-Doped Magnesium Phosphate Cement (ZMPC): A Novel Material for Orthopedic Bone Defect Repair.Biomedicines · 2024Article
- Genetic and Gene Expression Resources for Osteoporosis and Bone Biology Research.Current osteoporosis reports · 2023Review
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- The dual role of autophagy in periprosthetic osteolysis.Frontiers in cell and developmental biology · 2023Review
- Sexing Bones: Improving Transparency of Sex Reporting to Address Bias Within Preclinical Studies.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Glucosamine delays the progression of osteoporosis in senile mice by promoting osteoblast autophagy.Nutrition & metabolism · 2022Article
- Matrix Vesicle-Mediated Mineralization and Osteocytic Regulation of Bone Mineralization.International journal of molecular sciences · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mineralized bone forms when collagen-containing osteoid accrues mineral crystals. This is initiated rapidly (primary mineralization), and continues slowly (secondary mineralization) until bone is remodeled. The interconnected osteocyte network within the bone matrix differentiates from bone-forming osteoblasts; although osteoblast differentiation requires EphrinB2, osteocytes retain its expression. Here we report brittle bones in mice with osteocyte-targeted EphrinB2 deletion. This is not caused by low bone mass, but by defective bone material. While osteoid mineralization is initiated at normal rate, mineral accrual is accelerated, indicating that EphrinB2 in osteocytes limits mineral accumulation. No known regulators of mineralization are modified in the brittle cortical bone but a cluster of autophagy-associated genes are dysregulated. EphrinB2-deficient osteocytes displayed more autophagosomes in vivo and in vitro, and EphrinB2-Fc treatment suppresses autophagy in a RhoA-ROCK dependent manner. We conclude that secondary mineralization involves EphrinB2-RhoA-limited autophagy in osteocytes, and disruption leads to a bone fragility independent of bone mass.
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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.