ArticleOxidative medicine and cellular longevity2021
Long Noncoding RNA ANPODRT Overexpression Protects Nucleus Pulposus Cells from Oxidative Stress and Apoptosis by Activating Keap1-Nrf2 Signaling.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- Antioxidant Nanotherapies for Intervertebral Disk Degeneration: Progress and Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- CDC25C downregulation suppresses HCC growth via mitochondrial stress-induced autophagy and apoptosis.Scientific reports · 2026Article
- Astragalus Polysaccharide Enhances O-GlcNAcylation Through OGT to Improve Intervertebral Disc Degeneration in Rats.Journal of cellular and molecular medicine · 2025Article
- lncRNAs as prognostic markers and therapeutic targets in cuproptosis-mediated cancer.Clinical and experimental medicine · 2024Review
- Glutathione: A Key Regulator of Extracellular Matrix and Cell Death in Intervertebral Disc Degeneration.Mediators of inflammation · 2024Review
- Oxidative stress in intervertebral disc degeneration: Molecular mechanisms, pathogenesis and treatment.Cell proliferation · 2023Review
- Polyphyllin I suppressed the apoptosis of intervertebral disc nucleus pulposus cells induced by IL-1β by miR-503-5p/Bcl-2 axis.Journal of orthopaedic surgery and research · 2023Article
- Astragaloside IV attenuates IL-1β-induced intervertebral disc degeneration through inhibition of the NF-κB pathway.Journal of orthopaedic surgery and research · 2022Article
- Regulated cell death: Implications for intervertebral disc degeneration and therapy.Journal of orthopaedic translation · 2022Review
- The Nrf2 antioxidant defense system in intervertebral disc degeneration: Molecular insights.Experimental & molecular medicine · 2022Review
- Hsa_circ_0134111 promotes intervertebral disc degeneration via sponging miR-578.Cell death discovery · 2022Article
- Oxidative Stress Aggravates Apoptosis of Nucleus Pulposus Cells through mOxidative medicine and cellular longevity · 2022Article
- Maltol Promotes Mitophagy and Inhibits Oxidative Stress via the Nrf2/PINK1/Parkin Pathway after Spinal Cord Injury.Oxidative medicine and cellular longevity · 2022Article
- Silencing ATF3 Might Delay TBHP-Induced Intervertebral Disc Degeneration by Repressing NPC Ferroptosis, Apoptosis, and ECM Degradation.Oxidative medicine and cellular longevity · 2022Article
- Bone Marrow Mesenchymal Stem Cell-Derived Extracellular Vesicles Carrying circ_0050205 Attenuate Intervertebral Disc Degeneration.Oxidative medicine and cellular longevity · 2022Article
- Long non-coding RNAs LINC00689 inhibits the apoptosis of human nucleus pulposus cells via miR-3127-5p/ATG7 axis-mediated autophagy.Open medicine (Warsaw, Poland) · 2022Article
- The potential mechanisms and application prospects of non-coding RNAs in intervertebral disc degeneration.Frontiers in endocrinology · 2022Review
- LncRNAs as a new regulator of chronic musculoskeletal disorder.Cell proliferation · 2021Review
- An Oxidative Stress-Related Gene Pair (Frontiers in immunology · 2021Article
- Natural Products of Pharmacology and Mechanisms in Nucleus Pulposus Cells and Intervertebral Disc Degeneration.Evidence-based complementary and alternative medicine : eCAM · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Oxidative stress and subsequent nucleus pulposus (NP) cell apoptosis are important contributors to the development of intervertebral disc degeneration (IDD). Emerging evidences show that long noncoding RNAs (lncRNAs) play a role in the pathogenesis of IDD. In this study, we investigated the role of lncRNA ANPODRT (anti-NP cell oxidative damage-related transcript) in oxidative stress and apoptosis in human NP cells. We found that ANPODRT was downregulated in degenerative NP tissues and in NP cells treated with tert-butyl hydroperoxide (TBHP, the oxidative stress inducer). ANPODRT overexpression alleviated oxidative stress and apoptosis in NP cells exposed to TBHP, while ANPODRT knockdown exerted opposing effects. Mechanistically, ANPODRT facilitated nuclear factor E2-related factor 2 (Nrf2) accumulation and nuclear translocation and activated its target genes by disrupting the kelch-like ECH-associated protein 1- (Keap1-) Nrf2 association in NP cells. Nrf2 knockdown abolished the antioxidative stress and antiapoptotic effects of ANPODRT in NP cells treated with TBHP. Collectively, our findings suggest that ANPODRT protects NP cells from oxidative stress and apoptosis, at least partially, by activating Nrf2 signaling, implying that ANPODRT may be a potential therapeutic target for IDD.
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