ArticleInflammation2023
SPI1 Regulates the Progression of Ankylosing Spondylitis by Modulating TLR5 via NF-κB Signaling.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed, 14 citations in OpenAlex.
- USP22 alleviates oxidative stress-induced BMSCs senescence by stabilizing SPI1 protein.Molecular genetics and genomics : MGG · 2026Article
- Transcriptomic Profiling of Toxic Copper Overload Induced by CuO Nanoparticles or Copper Ions in Human Lung Epithelial and Liver Cells.Nanomaterials (Basel, Switzerland) · 2026Article
- Characterization of immune features and discovery of potential biomarkers for ankylosing spondylitis using deep plasma proteomics.Journal of advanced research · 2026Article
- Multiomics combined drugs to explore the potential mechanism and treatment of ankylosing spondylitis.Journal of orthopaedic surgery and research · 2026Article
- Monocyte/macrophage-derived NLRP3 Promotes the Onset and Progression of Ankylosing Spondylitis Via the NOD-like Receptor Pathway.Journal of clinical immunology · 2025Article
- Plasma Exosomes Derived from Patients with Primary Immune Thrombocytopenia Attenuate TBX21Inflammation · 2025Article
- The SPI1/SMAD5 cascade in the promoting effect of icariin on osteogenic differentiation of MC3T3-E1 cells: a mechanism study.Journal of orthopaedic surgery and research · 2024Article
- Exploration of the combined role of immune checkpoints and immune cells in the diagnosis and treatment of ankylosing spondylitis: a preliminary study immune checkpoints in ankylosing spondylitis.Arthritis research & therapy · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ankylosing spondylitis (AS) is an autoimmune disease which associated with inflammation of the spinal joints. Enhanced osteogenic differentiation was observed in AS; however, the underlying mechanism remains undefined. A cohort of AS (n = 15) and patients with traumatic fracture (n = 15) were recruited to this study. Fibroblasts were isolated, and characterized by H&E and immunocytochemistry (ICC) analysis. The expression and secretion of key molecules were detected by qRT-PCR, western blot, immunofluorescence (IF), and ELISA. Calcium deposition and alkaline phosphatase (ALP) activity were monitored by Alizarin Red S and ALP staining. The direct association between Spi-1 proto-oncogene (SPI1) and toll-like receptor 5 (TLR5) promoter was assessed by ChIP assay. AS fibroblasts was successfully isolated and exhibited osteogenic differentiation potentials. SPI1 was elevated in AS fibroblasts, and silencing of SPI1 inhibited osteogenic differentiation of AS fibroblasts. Mechanistic study showed that SPI1 acted as a transcriptional activator of TLR5. Knockdown of TLR5 suppressed osteogenic differentiation of AS fibroblasts via nuclear factor kappa B (NF-κB) signaling. Rescue experiments revealed that overexpression of TLR5 reversed SPI1 knockdown-suppressed osteogenic differentiation via NF-κB signaling. SPI1 regulated the progression of AS by modulating TLR5 via NF-κB signaling.
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.