ArticleHuman genomics2025
Potential involvement of the KLF2-GPX4 axis in ferroptosis during S.aureus-induced osteomyelitis.
Article in Human genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundIncreasing evidence suggests that ferroptosis plays a pivotal role in Staphylococcus aureus (S. aureus)-induced osteomyelitis. However, the regulatory mechanisms underlying ferroptosis-related genes (FRGs) in osteomyelitis remain poorly understood. This study aimed to identify key FRGs and elucidate their regulatory roles in osteomyelitis.
methodsKey FRGs were identified using least absolute shrinkage and selection operator (LASSO) logistic regression and support vector machine-recursive feature elimination (SVM-RFE) algorithms based on transcriptomic data from the Gene Expression Omnibus (GEO) database. Bone marrow mesenchymal stromal cells (BMSCs) were isolated, characterized, and infected with S. aureus protein A (SpA) to construct an in vitro model. Cell viability, osteogenic differentiation, inflammation, and gene expression were assessed using Cell Counting Kit-8 (CCK-8), Alizarin Red S staining, enzyme-linked immunosorbent assay (ELISA), and quantitative reverse transcription polymerase chain reaction (qRT-PCR). In vivo, a mouse model of S. aureus-induced osteomyelitis was established, and the role of KLF2 was examined by micro-computed tomography (micro-CT), ELISA, histological staining, immunohistochemistry, immunofluorescence, and qRT-PCR.
resultsA total of 683 differentially expressed FRGs were identified. Ten candidate biomarkers were screened using LASSO and SVM-RFE, of which TXN, KLF2, HSPA8, CCT3, and AKR1C3 were consistently validated across training and validation datasets. These genes were associated with immune regulation, protein synthesis, and multiple ribosome- and metabolism-related pathways. In vitro, SpA treatment increased inflammation response, reduced BMSC proliferation and osteogenic differentiation, upregulated HSPA8, TXN, and CCT3, and downregulated KLF2 and its putative downstream target GPX4. In vivo, KLF2 overexpression alleviated S. aureus-induced bone loss, inflammation, and ferroptosis, while promoting angiogenesis and osteogenesis, in part through modulation of GPX4.
conclusionThis study highlights KLF2 as a potential protective factor in S. aureus-induced osteomyelitis, possibly by regulating GPX4 and ferroptosis.
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.