ArticleBone research2014
Hypoxia-inducible factor-1α restricts the anabolic actions of parathyroid hormone.
Article in Bone research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Differential but complementary roles of HIF-1α and HIF-2α in the regulation of bone homeostasis.Communications biology · 2024Article
- The Bioactive Compounds ofPharmaceuticals (Basel, Switzerland) · 2024Article
- Positive Feedback Regulation of Circular RNA Hsa_circ_0000566 and HIF-1α promotes Osteosarcoma Progression and Glycolysis Metabolism.Aging and disease · 2023Article
- Hypoxia-inducible factor signaling in vascular calcification in chronic kidney disease patients.Journal of nephrology · 2022Review
- Contrasting effects ofeLife · 2022Article
- Bioceramic Scaffolds with Antioxidative Functions for ROS Scavenging and Osteochondral Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Effects of hypoxia on bone metabolism and anemia in patients with chronic kidney disease.World journal of clinical cases · 2021Article
- Anabolic actions of PTH in murine models: two decades of insights.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Article
- Oxygen desaturation during the 6-min walk test as a risk for osteoporosis in non-cystic fibrosis bronchiectasis.BMC pulmonary medicine · 2019Article
- NFAT1 protects articular cartilage against osteoarthritic degradation by directly regulating transcription of specific anabolic and catabolic genes.Bone & joint research · 2019Article
- Hypoxia Signaling in the Skeleton: Implications for Bone Health.Current osteoporosis reports · 2019Review
- Hypoxia enhances angiogenesis in an adipose-derived stromal cell/endothelial cell co-culture 3D gel model.Cell proliferation · 2016Article
- Physiological oxygen tension modulates soluble growth factor profile after crosstalk between chondrocytes and osteoblasts.Cell proliferation · 2016Article
- Gene profile of soluble growth factors involved in angiogenesis, in an adipose-derived stromal cell/endothelial cell co-culture, 3D gel model.Cell proliferation · 2015Article
- Direct or indirect stimulation of adenosine A2A receptors enhances bone regeneration as well as bone morphogenetic protein-2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Obstructive sleep apnea and metabolic bone disease: insights into the relationship between bone and sleep.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The hypoxia inducible factors (Hifs) are evolutionarily conserved transcriptional factors that control homeostatic responses to low oxygen. In developing bone, Hif-1 generated signals induce angiogenesis necessary for osteoblast specification, but in mature bone, loss of Hif-1 in osteoblasts resulted in a more rapid accumulation of bone. These findings suggested that Hif-1 exerts distinct developmental functions and acts as a negative regulator of bone formation. To investigate the function of Hif-1α in osteoanabolic signaling, we assessed the effect of Hif-1α loss-of-function on bone formation in response to intermittent parathyroid hormone (PTH). Mice lacking Hif-1α in osteoblasts and osteocytes form more bone in response to PTH, likely through a larger increase in osteoblast activity and increased sensitivity to the hormone. Consistent with this effect, exposure of primary mouse osteoblasts to PTH resulted in the rapid induction of Hif-1α protein levels via a post-transcriptional mechanism. The enhanced anabolic response appears to result from the removal of Hif-1α-mediated suppression of β-catenin transcriptional activity. Together, these data indicate that Hif-1α functions in the mature skeleton to restrict osteoanabolic signaling. The availability of pharmacological agents that reduce Hif-1α function suggests the value in further exploration of this pathway to optimize the therapeutic benefits of PTH.
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.