ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2020
CTRP3 Regulates Endochondral Ossification and Bone Remodeling During Fracture Healing.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 20 citations in OpenAlex.
- CTRP10 is required for optimal motor function.The Journal of biological chemistry · 2026Article
- Panx3 deficiency in mice impairs bone fracture healing and causes transient hypoglycemia in neonatal animals.Molecular medicine (Cambridge, Mass.) · 2026Article
- Article
- gCTRP3 inhibits oophorectomy‑induced osteoporosis by activating the AMPK/SIRT1/Nrf2 signaling pathway in mice.Molecular medicine reports · 2024Article
- Pharmacological TRPC6 inhibition improves survival and muscle function in mice with Duchenne muscular dystrophy.JCI insight · 2022Article
- CTRP11 contributes modestly to systemic metabolism and energy balance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Plasma C1q/tumor necrosis factor-related protein-3 concentrations are associated with diabetic peripheral neuropathy.BMJ open diabetes research & care · 2022Article
- Notch signaling enhances bone regeneration in the zebrafish mandible.Development (Cambridge, England) · 2022Article
- Core-binding factor beta is required for osteoblast differentiation during fibula fracture healing.Journal of orthopaedic surgery and research · 2021Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
C1q/TNF-related protein 3 (CTRP3) is a cytokine known to regulate a variety of metabolic processes. Though previously undescribed in the context of bone regeneration, high throughput gene expression experiments in mice identified CTRP3 as one of the most highly upregulated genes in fracture callus tissue. Hypothesizing a positive regulatory role for CTRP3 in bone regeneration, we phenotyped skeletal development and fracture healing in CTRP3 knockout (KO) and CTRP3 overexpressing transgenic (TG) mice relative to wild-type (WT) control animals. CTRP3 KO mice experienced delayed endochondral fracture healing, resulting in abnormal mineral distribution, the presence of periosteal marrow compartments, and a nonunion-like state. Decreased osteoclast number was also observed in CTRP3 KO mice, whereas CTRP3 TG mice underwent accelerated callus remodeling. Gene expression profiling revealed a broad impact on osteoblast/osteoclast lineage commitment and metabolism, including arrested progression toward mature skeletal lineages in the KO group. A single systemic injection of CTRP3 protein at the time of fracture was insufficient to phenocopy the chronic TG healing response in WT mice. By associating CTRP3 levels with fracture healing progression, these data identify a novel protein family with potential therapeutic and diagnostic value. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:00-19966, 2020.
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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.