ArticleCytotechnology2025
IGFBP7 inhibition relieves LPS induced nucleus pulposus cell injury by regulating the ERK1/2 pathway.
Article in Cytotechnology, 2025. 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) and its secondary morbidity cause a severe reduction in quality of life. NP cells play a key role in the development of IDD. IGFBP7 plays a role in numerous diseases, especially in orthopedic disorders, but its role and mechanism for IDD are not clear. The aim of this study was to investigate the role and mechanism of IGFBP7 in a cellular model of LPS-induced IDD. Human primary NP cells were cultured, and subsequently, LPS-stimulated human NP cells were employed to establish an IDD cell model. RT-qPCR and western blot assay were conducted to assess the expression of IGFBP7 in NP cells. A small interfering RNA targeting IGFBP7 (IGFBP7-siRNA) was used to explore the role of IGFBP7 in LPS-treated human NP cells. The viability and apoptosis levels of these cells were then evaluated using MTT assay and flow cytometry analysis. The secretion of TNF-α, IL-6, and IL-1β was calculated by ELISA. RT-qPCR and western blot assay were also utilized to measure the expression levels of Bax, Bcl-2, aggrecan, and type II collagen. Furthermore, western blot analysis was employed to detect the phosphorylation levels of ERK1/2 proteins. To explore the role of the ERK1/2 pathway in NP cells, LM22B-10, an ERK activator, was applied. IGFBP7 expression was significantly elevated in LPS-stimulated human NP cells to approximately 3 folds of control levels. LPS significantly inhibited the viability of human NP cells and promoted the level of apoptosis and inflammatory factor secretion. LPS markedly induced the expression of Bax in human NP cells, while suppressed the abundance of Bcl-2, aggrecan, and collagen type II. LPS significantly activated the ERK1/2 pathway in human NP cells, promoting an increase in ERK1/2 phosphorylation levels. All of these phenomena were reversed by IGFBP7-siRNA. LM22B-10 could significantly reverse the effects of IGFBP7-siRNA on LPS-induced human NP cells. Silencing of IGFBP7 could mitigate apoptosis and inflammatory response triggered by LPS in human NP cells by suppressing the ERK1/2 pathway, suggesting a protective role in IDD. IGFBP7 is a potential therapeutic target for IDD.
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.