ArticleCommunications biology2024
Endothelial SMAD1/5 signaling couples angiogenesis to osteogenesis in juvenile bone.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- The transcriptional atlas, intercellular communication, and metabolic reprogramming of the cartilage and synovium in osteoarthritis patients with diabetes mellitus : a multiomics study.Bone & joint research · 2026Article
- Targeting endoplasmic reticulum stress and YAP/TAZ-SMAD1/5 signaling to ameliorate endothelial dysfunction in diabetes.Acta pharmacologica Sinica · 2026Article
- Bioinspired 3D Bone Model: Mimicking the Cortical-Spongy Bone Architecture and Biology for Enhanced Physiological Representation of Bone.ACS biomaterials science & engineering · 2025Article
- Communication between endothelial cells and osteoblasts in regulation of bone homeostasis: Notch players.Stem cell research & therapy · 2025Review
- Delayed Administration of IGFBP7 Improved Bone Defect Healing via ZO-1 Dependent Vessel Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- In-silico analysis predicts disruption of normal angiogenesis as a causative factor in osteoporosis pathogenesis.BMC genomic data · 2024Article
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8 authors at 6 institutions in 3 countries.
Funding
Abstract
Skeletal development depends on coordinated angiogenesis and osteogenesis. Bone morphogenetic proteins direct bone formation in part by activating SMAD1/5 signaling in osteoblasts. However, the role of SMAD1/5 in skeletal endothelium is unknown. Here, we found that endothelial cell-conditional SMAD1/5 depletion in juvenile mice caused metaphyseal and diaphyseal hypervascularity, resulting in altered trabecular and cortical bone formation. SMAD1/5 depletion induced excessive sprouting and disrupting the morphology of the metaphyseal vessels, with impaired anastomotic loop formation at the chondro-osseous junction. Endothelial SMAD1/5 depletion impaired growth plate resorption and, upon long-term depletion, abrogated osteoprogenitor recruitment to the primary spongiosa. Finally, in the diaphysis, endothelial SMAD1/5 activity was necessary to maintain the sinusoidal phenotype, with SMAD1/5 depletion inducing formation of large vascular loops and elevated vascular permeability. Together, endothelial SMAD1/5 activity sustains skeletal vascular morphogenesis and function and coordinates growth plate remodeling and osteoprogenitor recruitment dynamics in juvenile mouse bone.
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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.