ArticleWorld journal of stem cells2023
Quercetin ameliorates oxidative stress-induced senescence in rat nucleus pulposus-derived mesenchymal stem cells
Article in World journal of stem cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
The trial behind it
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Who cites it
27 citing papers in PubMed, 29 citations in OpenAlex.
- Integrated bioinformatics, single-cell analysis, and experimental validation identify quercetin as a potential therapeutic candidate for intervertebral disc degeneration.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Quercetin as a Multifunctional Flavonol: Molecular Insights and Therapeutic Applications.Molecules (Basel, Switzerland) · 2026Review
- Nuciferine-Loaded Lipid Nanoparticle Microneedles Alleviate Intervertebral Disc Degeneration by Restoring Nucleus Pulposus Cell Homeostasis.Pharmaceutics · 2026Article
- Review
- The role and potential therapeutic intervention of cellular senescence in intervertebral disc degeneration.Genes & diseases · 2026Review
- Calming sterile inflammation in intervertebral disc degeneration: taurine disrupts mitochondria-cGAS-STING signaling via autophagy enhancement.Precision clinical medicine · 2026Article
- Superoxide dismutase in intervertebral disc degeneration: from pathophysiological mechanism to therapeutic strategies.Molecular biology reports · 2026Review
- Awakening endogenous repair: salidroside boosts mitophagy in NPMSCs via SIRT1/FOXO3 to combat intervertebral disc degeneration.Stem cell research & therapy · 2026Article
- From multi-target mechanisms to clinical translation: the analgesic potential of quercetin.Frontiers in pharmacology · 2026Review
- Natural Products as Anti-Senescence-Associated Secretory Phenotype (SASP) Agents.Current medicinal chemistry · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Utilising bioinformatics and molecular docking technology to explore the underlying mechanisms of intervertebral disc degeneration with potential therapeutic drugs and formulas.Journal of global health · 2025Article
- Review
- Article
- Quercetin nanoformulation-embedded hydrogel inhibits osteopontin mediated ferroptosis for intervertebral disc degeneration alleviation.Journal of nanobiotechnology · 2025Article
- Article
- CircSPG21 ameliorates oxidative stress-induced senescence in nucleus pulposus-derived mesenchymal stem cells and mitigates intervertebral disc degeneration through the miR-217/SIRT1 axis and mitophagy.Stem cell research & therapy · 2025Article
- Diabetes mellitus and glymphatic dysfunction: Roles for oxidative stress, mitochondria, circadian rhythm, artificial intelligence, and imaging.World journal of diabetes · 2025Review
- Bioactive metabolites of botanical drugs in the treatment of intervertebral disc degeneration-a review of promising therapeutic candidate.Frontiers in pharmacology · 2025Review
- Natural products for intervertebral disc degeneration: mechanistic insights and therapeutic potentials.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntervertebral disc degeneration (IDD) is a main contributor to low back pain. Oxidative stress, which is highly associated with the progression of IDD, increases senescence of nucleus pulposus-derived mesenchymal stem cells (NPMSCs) and weakens the differentiation ability of NPMSCs in degenerated intervertebral discs (IVDs). Quercetin (Que) has been demonstrated to reduce oxidative stress in diverse degenerative diseases.
aimTo investigate the role of Que in oxidative stress-induced NPMSC damage and to elucidate the underlying mechanism.
methods
resultsWe found that TBHP can cause NPMSCs senescence changes, such as reduced cell proliferation ability, increased SA-β-Gal activity, cell cycle arrest, the accumulation of ROS, and increased expression of senescence-related proteins. While abovementioned senescence indicators were significantly alleviated by Que treatment. Que decreased the expression levels of senescence-related proteins (p16, p21, and p53) and senescence-associated secreted phenotype (SASP), including IL-1β, IL-6, and MMP-13, and it increased the expression of SIRT1. In addition, the protective effects of Que on cell senescence were partially reversed by miR-34a-5p overexpression and SIRT1 knockdown.
conclusionIn summary, the present study provides evidence that Que reduces oxidative stress-induced senescence of NPMSCs
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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.