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Updated: Jun 30, 2025

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
FOXQ1 inhibits the progression of osteoarthritis by regulating pyroptosis
Zhihuan Luo1, Hui Zeng1, Kanghua Yang1
1Department of Sports Medicine, Ganzhou People’s Hospital, Ganzhou 341000, Jiangxi Province, China.
Background:
Osteoarthritis (OA) is the most common age-related joint disease, and the NLRP3-induced pyroptosis has been demonstrated in its progression. The upstream molecules or specific mechanisms controlling NLRP3 and pyroptosis in OA remain unclear.
Methods:
Transcriptome sequencing was performed in the OA mice model, and the expression levels of differentially expressed genes were assessed by qRT-PCR. The cell model was constructed by IL-1β-induced ATDC5 cells. The cell proliferation was examined using CCK-8 assay, and apoptosis was tested using flow cytometry. Western blot was used in protein inspection, and ELISA was used in inflammatory response evaluation.
Results:
Compared with the control group, there were 229 up-regulated and 32 down-regulated genes in model group. We detected that FOXQ1 was down-regulated in the OA mice model, improved proliferation, and restrained apoptosis of chondrocytes. Over-expression of FOXQ1 could inhibit pyroptosis-related proteins and inflammatory cytokines, containing NLRP3, Caspase-1, GSDMD, IL-6, IL-18, and TNF-α, and in contrast, FOXQ1 silencing exerted the opposite trend.
Conclusions:
FOXQ1 may inhibit OA progression via down-regulating NLRP3-induced pyroptosis in the present study.
Insights
Forkhead box Q1 (FOXQ1) inhibits osteoarthritis progression by suppressing NLRP3-induced pyroptosis. This study reveals FOXQ1 as a potential therapeutic target for managing this common age-related joint disease.
Area of Science:
- Biomedical research
- Molecular biology
- Genetics
Background:
- Osteoarthritis (OA) is a prevalent age-related joint disease.
- NLRP3-induced pyroptosis is implicated in OA pathogenesis.
- The regulatory mechanisms of NLRP3 and pyroptosis in OA are not fully understood.
Purpose of the Study:
- To investigate the role of FOXQ1 in osteoarthritis.
- To elucidate the mechanism by which FOXQ1 affects chondrocyte pyroptosis and OA progression.
Main Methods:
- Transcriptome sequencing in an OA mouse model.
- Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
- In vitro cell models (IL-1β-induced ATDC5 cells) to assess cell proliferation (CCK-8 assay), apoptosis (flow cytometry), protein expression (Western blot), and inflammatory responses (ELISA).
Main Results:
- FOXQ1 was found to be downregulated in the OA mouse model.
- Overexpression of FOXQ1 promoted chondrocyte proliferation and inhibited apoptosis.
- FOXQ1 suppressed key pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD) and inflammatory cytokines (IL-6, IL-18, TNF-α).
Conclusions:
- FOXQ1 plays an inhibitory role in osteoarthritis progression.
- The mechanism involves the downregulation of NLRP3-induced pyroptosis.
- FOXQ1 represents a potential therapeutic target for osteoarthritis.
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