ArticleNature cell biology2019
Endothelial proteolytic activity and interaction with non-resorbing osteoclasts mediate bone elongation.
Article in Nature cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 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
122 citing papers in PubMed, 1 synthesis or guideline pooled it, 201 citations in OpenAlex.
- Insights into the mechanism of vascular endothelial cells on bone biology.Bioscience reports · 2021Pooled it
- Vascular-lymphatic dual circulation in bone health and disease: Mechanistic coupling and translational therapeutics.Journal of orthopaedic translation · 2026Review
- Repeated social defeat causes bone loss from mouse femur.Brain, behavior, & immunity - health · 2026Article
- Sulfated polysaccharides target RANK Lys97 to inhibit osteoclast differentiation and reverse osteoporosis.Nature biomedical engineering · 2026Article
- Blood and lymphatic vascular network in bone injury repair: from molecular mechanisms to therapeutic strategies.Science China. Life sciences · 2026Review
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- Soluble Epoxide Hydrolase Inhibition Regulates Septoclast Activity to Promote Long Bone Growth and Fracture Healing by Enhancing Endothelial-to-Mesenchymal Notch Signalling.Cell proliferation · 2026Article
- Advances in GelMA Hydrogel-Enabled Angiogenic-Osteogenic Coupling: From Structural Programming to Exogenous Cue Synergy.Journal of functional biomaterials · 2026Review
- Recapitulating Endochondral Ossification for Bone Repair: From Development to Engineering Strategy.Advanced healthcare materials · 2026Review
- Development-based In Vivo Bioreactor Strategy for Challenging Senescent Bone Reconstruction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Crosstalk between bone and vasculature within bone.Fundamental research · 2026Review
- Vascular and musculoskeletal interactions: structure, function, and therapeutic strategies for sarcopenia and osteoporosis.MedScience · 2026Review
- Endothelial diversity in bone vasculature coordinates osteogenesis and hematopoiesis.Journal of bone and mineral metabolism · 2026Review
- Traditional Chinese Medicine for osteoporosis management: from molecular mechanisms to drug discovery.Chinese medicine · 2026Review
- Modeling the chondrocyte-derived osteoblasts formation process reveals its molecular signature and regulation network.Bone research · 2026Article
- Sulfated chitosan mitigates acute lung injury induced bone loss via immunoregulation.Bone research · 2026Article
- APEX1, a transcriptional hub for endochondral ossification and fracture repair.Bone research · 2026Article
- The developmental remodeling front: resorptive cell-vascular coupling at the chondro-osseous junction.Frontiers in cell and developmental biology · 2026Review
- Descendants of hypertrophic chondrocytes promote angiogenesis by secreting THBS4 during bone growth and injury repair.Bone research · 2025Article
- Tartrate-Resistant Acid Phosphatase-Positive Cells: Putative Mediators of Peri-Implant Bone Healing.Journal of periodontal research · 2025Article
62 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Growth plate cartilage contributes to the generation of a large variety of shapes and sizes of skeletal elements in the mammalian system. The removal of cartilage and how this process regulates bone shape are not well understood. Here we identify a non-bone-resorbing osteoclast subtype termed vessel-associated osteoclast (VAO). Endothelial cells at the bone/cartilage interface support VAOs through a RANKL-RANK signalling mechanism. In contrast to classical bone-associated osteoclasts, VAOs are dispensable for cartilage resorption and regulate anastomoses of type H vessels. Remarkably, proteinases including matrix metalloproteinase-9 (Mmp9) released from endothelial cells, not osteoclasts, are essential for resorbing cartilage to lead directional bone growth. Importantly, disrupting the orientation of angiogenic blood vessels by misdirecting them results in contorted bone shape. This study identifies proteolytic functions of endothelial cells in cartilage and provides a framework to explore tissue-lytic features of blood vessels in fracture healing, arthritis and cancer.
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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.