ArticleThe Journal of biological chemistry2011
Hypoxia-inducible factor-1α protein negatively regulates load-induced bone formation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Oxygen Sensing in Osteocytes: From Physiology to Age-related Osteoporosis.Current osteoporosis reports · 2025Review
- Differential but complementary roles of HIF-1α and HIF-2α in the regulation of bone homeostasis.Communications biology · 2024Article
- Hypoxia Pathway in Osteoporosis: Laboratory Data for Clinical Prospects.International journal of environmental research and public health · 2023Review
- Type H vessels: functions in bone development and diseases.Frontiers in cell and developmental biology · 2023Review
- Protein Kinase G2 Is Essential for Skeletal Homeostasis and Adaptation to Mechanical Loading in Male but Not Female Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Review
- Macrophages in heterotopic ossification: from mechanisms to therapy.NPJ Regenerative medicine · 2021Review
- Physical Activity and Bone Vascularization: A Way to Explore in Bone Repair Context?Life (Basel, Switzerland) · 2021Review
- Upregulated proteoglycan-related signaling pathways in fluid flow shear stress-treated podocytes.American journal of physiology. Renal physiology · 2020Article
- CSF-1 in Osteocytes Inhibits Nox4-mediated Oxidative Stress and Promotes Normal Bone Homeostasis.JBMR plus · 2020Article
- Osteocyte-Mediated Translation of Mechanical Stimuli to Cellular Signaling and Its Role in Bone and Non-bone-Related Clinical Complications.Current osteoporosis reports · 2020Review
- Type H blood vessels in bone modeling and remodeling.Theranostics · 2020Review
- Mechanical force promotes the proliferation and extracellular matrix synthesis of human gingival fibroblasts cultured on 3D PLGA scaffolds via TGF‑β expression.Molecular medicine reports · 2019Article
- Hypoxia Signaling in the Skeleton: Implications for Bone Health.Current osteoporosis reports · 2019Review
- Article
- Osteoblast Differentiation and Bone Matrix Formation In Vivo and In Vitro.Tissue engineering. Part B, Reviews · 2017Article
- Vascular patterning in human heterotopic ossification.Human pathology · 2017Article
- Overexpression of miR-223 Tips the Balance of Pro- and Anti-hypertrophic Signaling Cascades toward Physiologic Cardiac Hypertrophy.The Journal of biological chemistry · 2016Article
- Physiological oxygen tension modulates soluble growth factor profile after crosstalk between chondrocytes and osteoblasts.Cell proliferation · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Mechanical loads induce profound anabolic effects in the skeleton, but the molecular mechanisms that transduce such signals are still poorly understood. In this study, we demonstrate that the hypoxia-inducible factor-1α (Hif-1α) is acutely up-regulated in response to exogenous mechanical stimuli secondary to prostanoid signaling and Akt/mTOR (mammalian target of rapamycin) activation. In this context, Hif-1α associates with β-catenin to inhibit Wnt target genes associated with bone anabolic activity. Mice lacking Hif-1α in osteoblasts and osteocytes form more bone when subjected to tibia loading as a result of increased osteoblast activity. Taken together, these studies indicate that Hif-1α serves as a negative regulator of skeletal mechanotransduction to suppress load-induced bone formation by altering the sensitivity of osteoblasts and osteocytes to mechanical signals.
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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.