ArticleImmunity, inflammation and disease2026
Thrombospondin-4 Regulates Lipopolysaccharide-Induced Apoptosis and Inflammation in Nucleus Pulposus Cells via the Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Thrombospondin-4 Regulates Lipopolysaccharide-Induced Apoptosis and Inflammation in Nucleus Pulposus Cells via the Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway.Immunity, inflammation and disease · 2026Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study investigated the expression profile of Thrombospondin-4 (THBS4) in intervertebral disc degeneration (IDD) and clarify its regulatory role in lipopolysaccharide (LPS)-induced apoptosis and inflammation in nucleus pulposus cells (NPCs) via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway.
methodsIDD-related differentially expressed genes were screened through the integration of GeneCards and the Gene Expression Omnibus (GEO) database (GSE186542), followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to explore potential signaling mechanisms. An in vitro inflammatory injury model was established using LPS-stimulated NPCs. The effects of THBS4 overexpression on cell proliferation, apoptosis, inflammatory cytokine secretion, and extracellular matrix protein expression were evaluated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blotting, 5-ethynyl-2'-deoxyuridine (EdU) assay, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). Additionally, the involvement of the PI3K/AKT pathway in mediating THBS4-related effects was confirmed using the PI3K inhibitor LY294002.
resultsBioinformatics analysis revealed that THBS4 was significantly downregulated in IDD and was closely linked to the PI3K/AKT pathway. Functional assays demonstrated that overexpression of THBS4 markedly enhanced NPCs proliferation, suppressed apoptosis, reduced the secretion of tumour necrosis factor alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6, and increased the expression of IL-10, Aggrecan, and Collagen type II. These protective effects were accompanied by activation of the PI3K/AKT pathway and were significantly reversed by LY294002 treatment.
conclusionTHBS4 alleviated LPS-induced damage in NPCs through the activation of the PI3K/AKT pathway, exerting anti-apoptotic and anti-inflammatory effects; the specific upstream molecular mechanism of PI3K/AKT activation by THBS4 requires further investigation. These findings suggested that THBS4 may serve as a potential therapeutic target for IDD treatment.
Indexed as
Identifiers
What Socratic 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 Socratic graph.