ArticleNature communications2019
TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Parathyroid Hormone Modulates Alveolar Bone Metabolism via Inducing Periodontal Ligament Stem Cells Aerobic Glycolysis.International dental journal · 2026Article
- Identification of plasma SEMA3E as the diagnostic biomarker for human epilepsy based on integrated bioinformatics analysis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- sLZIP functions as a key modulator of bone remodeling by regulating the crosstalk between osteoblasts and osteoclasts.Experimental & molecular medicine · 2025Article
- Lipopolysaccharide (LPS) induces sclerostin secretion by extracellular vesicle via TLR4/miR-92a-3p/PTEN/NF-κB signalling pathway in murine macrophage.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- The Progress of Immune Cells-induced Inflammatory Response in Gout.Current pharmaceutical design · 2025Review
- The Alterations in the Osteoimmune Microenvironment of STZ-Induced Type 2 Diabetic Mice:A Single-Cell RNA Sequencing Analysis.Journal of inflammation research · 2025Article
- Comprehensive analysis of mesenchymal cells reveals a dysregulated TGF-β/WNT/HOXB7 axis in patients with myelofibrosis.JCI insight · 2024Article
- Trajectory-centric framework TrajAtlas reveals multi-scale differentiation heterogeneity among cells, genes, and gene modules in osteogenesis.PLoS genetics · 2024Article
- Article
- Etiological Mechanisms and Genetic/Biological Modulation Related to PTH1R in Primary Failure of Tooth Eruption.Calcified tissue international · 2024Review
- Evaluating the association between lifestyle factors and heel bone mineral density in different inflammatory states.Heliyon · 2024Article
- Tgif1-deficiency impairs cytoskeletal architecture in osteoblasts by activating PAK3 signaling.eLife · 2024Article
- M2 macrophages secrete glutamate-containing extracellular vesicles to alleviate osteoporosis by reshaping osteoclast precursor fate.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Review
- NPRC deletion attenuates cardiac fibrosis in diabetic mice by activating PKA/PKG and inhibiting TGF-β1/Smad pathways.Science advances · 2023Article
- Article
- Antagonizing microRNA-19a/b augments PTH anabolic action and restores bone mass in osteoporosis in mice.EMBO molecular medicine · 2022Article
- Procalcitonin is expressed in osteoblasts and limits bone resorption through inhibition of macrophage migration during intermittent PTH treatment.Bone research · 2022Article
- Metabolic and Transcriptional Changes across Osteogenic Differentiation of Mesenchymal Stromal Cells.Bioengineering (Basel, Switzerland) · 2021Article
- Cytokine-scavenging nanodecoys reconstruct osteoclast/osteoblast balance toward the treatment of postmenopausal osteoporosis.Science advances · 2021Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
Abstract
Osteoporosis is caused by increased bone resorption and decreased bone formation. Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteoporosis. However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated. Here we show that the absence of the homeodomain protein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a reduced bone formation. Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3E (Sema3E), an osteoclast-inhibiting factor. Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice. Thus, our study identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH anabolic action. These insights contribute to a better understanding of bone metabolism and the anabolic function of PTH.
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Registered trials
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