ArticleAging2020
TNFAIP3 ameliorates the degeneration of inflammatory human nucleus pulposus cells by inhibiting mTOR signaling and promoting autophagy.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Transcriptome and m6A epitranscriptome profiling reveal CCL20 as a key mediator of inflammation in Staphylococcus aureus-induced bovine mastitis.BMC microbiology · 2026Article
- The Role of TFEB-Regulated Autophagy in Intervertebral Disc Degeneration and Its Therapeutic Potential.Journal of inflammation research · 2026Review
- Exosomal miRNA-25-3p from platelet-rich plasma alleviates chondrocyte pyroptosis and knee osteoarthritis by regulating MAP4K2/Hippo/TNFAIP3 pathway.Functional & integrative genomics · 2025Article
- Mapping the Potential Genes and Associated Pathways Involved in Long COVID-Associated Brain Fog Using Integrative Bioinformatics and Systems Biology Strategy.Molecular biotechnology · 2025Article
- Transcriptomic-based analysis of endometrial tissues from adenomyosis patients reveals significant inflammation biomarkers: A bioinformatics study.International journal of reproductive biomedicine · 2025Article
- Single-cell RNA sequencing of circulating immune cells supports inhibition ofFrontiers in immunology · 2025Article
- 17β-estradiol maintains extracellular matrix homeostasis of nucleus pulposus cells by activating p70 S6K1 signaling pathway.Frontiers in cell and developmental biology · 2025Article
- Targeting nucleus pulposus cell death in the treatment of intervertebral disc degeneration.JOR spine · 2024Review
- Article
- Comparative Study on the Mechanism of Macrophage Activation Induced by Polysaccharides from Fresh and Dried Longan.Nutrients · 2024Article
- Examining the Potential of Vitamin C Supplementation in Tissue-Engineered Equine Superficial Digital Flexor Tendon Constructs.International journal of molecular sciences · 2023Article
- A Model of iPSC-Derived Macrophages withInternational journal of molecular sciences · 2023Article
- A20 ameliorates disc degeneration by suppressing mTOR/BNIP3 axis-mediated mitophagy.Genes & genomics · 2023Article
- Emerging role and therapeutic implication of mTOR signalling in intervertebral disc degeneration.Cell proliferation · 2023Review
- A20 attenuates pyroptosis and apoptosis in nucleus pulposus cells via promoting mitophagy and stabilizing mitochondrial dynamics.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is involved in degenerative diseases such as osteoarthritis and disc degeneration. Although, tumor necrosis factor α-induced protein 3 (TNFAIP3) is well-known as a key regulator of inflammation and autophagy, it is still not clear whether TNFAIP3 regulates autophagy to protect from human disc cells degeneration. We hypothesize that TNFAIP3 may also regulate autophagy to inhibit pro-inflammatory cytokines expression in human nucleus pulposus cells (NPCs). In this study, TNFAIP3 expression was increased in degenerative disc tissue as well as LPS-stimulated human NPCs, and the effect of TNFAIP3 in LPS-induced NPCs was further explored. The results demonstrated that pro-inflammatory cytokines expression in TNFAIP3-His cells was decreased, while it was increased in TNFAIP3-siRNA cells. Further molecular mechanism research showed that TNFAIP3-siRNA cells enhanced the phosphorylation of mammalian target of rapamycin (mTOR) and inhibited autophagy. Meanwhile, after treatment of TNFAIP3-siRNA cells with the mTOR inhibitor Torin1, the level of autophagy increased and the decrease of extracellular matrix was reversed. In summary, overexpressed TNFAIP3 can promote autophagy and reduce inflammation in LPS-induced human NPCs. Moreover, autophagy triggered by TNFAIP3 can ameliorate the degeneration of inflammatory human NPCs, providing a potential and an attractive therapeutic strategy for degenerative disease.
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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.