ArticlemSystems2022
Article in mSystems, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Metabolic flux analysis revealed key roles of ArcB in ADI pathway and IlvC in BCAA biosynthesis duringVirulence · 2026Article
- HIF-1α at the intersection of hypoxia, ferroptosis-associated stress, and cell death crosstalk in osteomyelitis.Frontiers in cell and developmental biology · 2026Review
- Article
- Dual stimulus-responsive dECM cryogel sequentially regulate bone microenvironment for one-step surgical therapy of chronic osteomyelitis.Materials today. Bio · 2025Article
- Insights into the potential role of BMSCs-exo delivered USP14 on SIRT1 deubiquitination in Staphylococcus aureus-induced model of osteomyelitis.Journal of orthopaedic surgery and research · 2025Article
- Implant-DerivedAntibiotics (Basel, Switzerland) · 2025Article
- Immune Checkpoint Molecules as Biomarkers ofbioRxiv : the preprint server for biology · 2024Article
- TRPA1 InfluencesInternational journal of molecular sciences · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Article
- Ultrastructural Evidence of Mitochondrial Dysfunction in Osteomyelitis Patients.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is unknown about the regulatory mechanisms underlying the pathogenesis of osteomyelitis induced by Staphylococcus aureus. Hypoxia-inducible factor-1α (HIF-1α) and transforming growth factor β1 (TGF-β1) were both upregulated in S. aureus-infected MC3T3-E1 cells and osteomyelitis patients. HIF-1α directly targets the hypoxia-responsive elements (HREs) of TGF-β1 mRNA to induce its expression. Silencing HIF-1α and TGF-β1, as well as treatment of hypoxia inhibitor IDF-11774, consistently elevated OPN and RUNX2 expression and alizarin Red S (ARS) and alkaline phosphatase (ALP) staining levels in MC3T3-E1 cells with S. aureus infection. S. aureus infection increased HIF-1α expression and serum TGF-β1 concentration in a mouse model of osteomyelitis. Hypoxia inhibitor IDF-11774 treatment reduced serum levels of interleukin (IL)-6, IL-1β, and C-reactive protein. Upon S. aureus infection, hypoxia was activated to trigger TGF-β1 upregulation through direct targeting of HRE on TGF-β1 mRNA by HIF-1α, eventually leading to osteomyelitis symptoms in terms of osteogenesis and mineralization deficiencies as well as elevated inflammation. This study hereby suggests a novel signaling cascade involving hypoxia/HIF-1α/TGF-β1 in osteomyelitis pathogenesis, which could potentially serve as a target for therapeutic measures.
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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.