ArticleJournal of cellular and molecular medicine2021
S100A9 induces nucleus pulposus cell degeneration through activation of the NF-κB signaling pathway.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 16 citations in OpenAlex.
- S100A9 regulates eosinophil extracellular trap and activates NF-κB signaling in endometrial cancer: a machine learning-based biomarker discovery.Cancer cell international · 2025Article
- Chronic Low Back Pain in Young Adults: Pathophysiological Aspects of Neuroinflammation and Degeneration.International journal of molecular sciences · 2025Article
- Identification of regulator gene and pathway in myocardial ischemia-reperfusion injury: a bioinformatics and biological validation study.Hereditas · 2025Article
- Advances in the study of S100A9 in cardiovascular diseases.Cell proliferation · 2024Review
- Tandem Mass Tag-Based Proteomic Analysis of Normal and Degenerated Human Intervertebral Discs.Journal of pain research · 2024Article
- Achilles' Heel-The Significance of Maintaining Microenvironmental Homeostasis in the Nucleus Pulposus for Intervertebral Discs.International journal of molecular sciences · 2023Review
- Review
- Article
- GSK-3β inhibition protects human nucleus pulposus cell against oxidative stress-inducing apoptosis through mitochondrial pathway.Molecular biology reports · 2022Article
- Significance of Immune-Related Genes in the Diagnosis and Classification of Intervertebral Disc Degeneration.Journal of immunology research · 2022Article
- S100A9 induces nucleus pulposus cell degeneration through activation of the NF-κB signaling pathway.Journal of cellular and molecular medicine · 2021Article
- miR-205-5p ameliorates podocyte injury in diabetic nephropathy by targeting vascular endothelial growth factor A.Science progressArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Oxidative stress in the lumbar disc leads to the degeneration of nucleus pulposus (NP). However, the molecular mechanisms underlying this process remain unclear. In this study, we delineated a key calcium-binding protein, S100A9, which was induced by oxidative stress and was highly expressed in the degenerative NP. Immunofluorescence staining and Western blotting revealed that S100A9 induced NP cell apoptosis in vitro by up-regulating the expression of pro-apoptotic markers, including cleaved caspase-3, cytochrome c and Bax. Moreover, RT-PCR analyses revealed that the expression of S100A9 caused NP matrix degradation by up-regulating the expression of matrix degradation enzymes and increased the inflammatory response by up-regulating cytokine expression. Therefore, S100A9 induced NP cell degeneration by exerting pro-apoptotic, pro-degradation and pro-inflammatory effects. The detailed mechanism underlying S100A9-induced NP degeneration was explored by administering SC75741, a specific NF-κB inhibitor in vitro. We concluded that S100A9 induced NP cell apoptosis, caused matrix degradation and amplified the inflammatory response through the activation of the NF-κB signalling pathway. Inhibition of these pro-apoptotic, pro-degradation and pro-inflammatory effects induced by S100A9 in NP may be a favourable therapeutic strategy to slow lumbar disc degeneration.
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.