ArticleBone2016
Sost, independent of the non-coding enhancer ECR5, is required for bone mechanoadaptation.
Article in Bone, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Methodological aspects ofJournal of musculoskeletal & neuronal interactions · 2023Pooled it
- Dissecting Hypoxia Inducible Factor-Driven High Bone Mass Phenotype in Mice Lacking Osteocytic Von Hippel-Lindau.JBMR plus · 2026Article
- Regional and Sexual Dimorphism in Murine Skeletal Responses to Osteocytic HIF Pathway Modulation.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Estrogenic prevention of luteinizing hormone releasing hormone agonist-induced bone loss.The Journal of endocrinology · 2025Article
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- Degradation-Resistant Hypoxia Inducible Factor-2α in Murine Osteocytes Promotes a High Bone Mass Phenotype.JBMR plus · 2023Article
- Exogenous Oncostatin M induces Cardiac Dysfunction, Musculoskeletal Atrophy, and Fibrosis.Cytokine · 2022Article
- Cortical bone adaptation to a moderate level of mechanical loading in male Sost deficient mice.Scientific reports · 2020Article
- A FAK/HDAC5 signaling axis controls osteocyte mechanotransduction.Nature communications · 2020Article
- Conditional Activation of NF-κB Inducing Kinase (NIK) in the Osteolineage Enhances Both Basal and Loading-Induced Bone Formation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Lrp4 Mediates Bone Homeostasis and Mechanotransduction through Interaction with Sclerostin In Vivo.iScience · 2019Article
- Expression of a Degradation-Resistant β-Catenin Mutant in Osteocytes Protects the Skeleton From Mechanodeprivation-Induced Bone Wasting.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Molecular and cellular mechanisms underlying the evolution of form and function in the amniote jaw.EvoDevo · 2019Review
- FGF and TGFβ signaling link form and function during jaw development and evolution.Developmental biology · 2018Article
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- Sost deficiency led to a greater cortical bone formation response to mechanical loading and altered gene expression.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Sclerostin (Sost) is a negative regulator of bone formation that acts upon the Wnt signaling pathway. Sost is mechanically regulated at both mRNA and protein level such that loading represses and unloading enhances Sost expression, in osteocytes and in circulation. The non-coding evolutionarily conserved enhancer ECR5 has been previously reported as a transcriptional regulatory element required for modulating Sost expression in osteocytes. Here we explored the mechanisms by which ECR5, or several other putative transcriptional enhancers regulate Sost expression, in response to mechanical stimulation. We found that in vivo ulna loading is equally osteoanabolic in wildtype and Sost
Indexed as
Identifiers
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.