ArticleAging cell2024
Nrf2 activation by pyrroloquinoline quinone inhibits natural aging-related intervertebral disk degeneration in mice.
Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- A Mechanism-Based Framework for Anti-Aging Strategies: From Metabolic Regulation to Senotherapy and Stem Cell-Based Interventions.Aging cell · 2026Review
- Pyrroloquinoline Quinone and NADPharmaceuticals (Basel, Switzerland) · 2026Review
- Antioxidant Nanotherapies for Intervertebral Disk Degeneration: Progress and Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Edaravone-based precision antioxidative therapy alleviates intervertebral disc degeneration via the Nrf2/Aldh3a1 axis.Materials today. Bio · 2026Article
- An integrated anti-aging framework targeting NADRedox biology · 2026Review
- Environmental Enrofloxacin Exposure as a Modifiable Driver of Mitochondria-Mediated Intestinal Aging and Barrier Dysfunction.Aging cell · 2026Article
- A ROS and pH dual - responsive hydrogel-nanoparticle system restores intervertebral disc and alleviates related pain by modulating senescence and panoptosis of nucleus pulposus cells.Materials today. Bio · 2026Article
- The Gut-Disc Axis: Mendelian Randomization Study Reveals Causal Effects of Gut Microbiota on Intervertebral Disc Degeneration Not Mediated by Systemic Inflammation.International journal of general medicine · 2026Article
- Review
- Pyrroloquinoline Quinone Is an Effective Senomorphic Agent to Target the Pro-Inflammatory Phenotype of Senescent Cells.Aging cell · 2025Article
- Cellular senescence and other age-related mechanisms in skeletal diseases.Bone research · 2025Review
- Current study on Pyrroloquinoline quinone (PQQ) therapeutic role in neurodegenerative diseases.Molecular biology reports · 2025Review
- Association between advanced fibrosis and epigenetic age acceleration among individuals with MASLD.Journal of gastroenterology · 2025Article
- Druggable Genome-Wide Mendelian Randomization Identifies Distinct Therapeutic Targets for Low Back Pain, Intervertebral Disk Degeneration, and Sciatica.Journal of pain research · 2025Article
- Nrf2 activation by pyrroloquinoline quinone inhibits natural aging-related intervertebral disk degeneration in mice.Aging cell · 2024Article
- Nanotechnology-Enhanced Pharmacotherapy for Intervertebral Disc Degeneration Treatment.International journal of nanomedicine · 2024Review
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Authors and funding
10 authors.
Funding
Abstract
Age-related intervertebral disk degeneration (IVDD) involves increased oxidative damage, cellular senescence, and matrix degradation. Pyrroloquinoline quinone (PQQ) is a water-soluble vitamin-like compound with strong anti-oxidant capacity. The goal of this study was to determine whether PQQ can prevent aging-related IVDD, and the underlying mechanism. Here, we found that dietary PQQ supplementation for 12 months alleviated IVDD phenotypes in aged mice, including increased disk height index and reduced histological scores and cell loss, without toxicity. Mechanistically, PQQ inhibited oxidative stress, cellular senescence, and senescence-associated secretory phenotype (SASP) in the nucleus pulposus and annulus fibrosus of aged mice. Similarly, PQQ protected against interleukin-1β-induced matrix degradation, reactive oxygen species accumulation, and senescence in human nucleus pulposus cells (NPCs) in vitro. Molecular docking predicted and biochemical assays validated that PQQ interacts with specific residues to dissociate the Keap1-Nrf2 complex, thereby increasing nuclear Nrf2 translocation and activation of Nrf2-ARE signaling. RNA sequencing and luciferase assays revealed Nrf2 can transcriptionally upregulate Wnt5a by binding to its promoter, while Wnt5a knockdown prevented PQQ inhibition of matrix metalloproteinase-13 in NPCs. Notably, PQQ supplementation failed to alleviate aging-associated IVDD phenotypes and oxidative stress in aged Nrf2 knockout mice, indicating Nrf2 is indispensable for PQQ bioactivities. Collectively, this study demonstrates Nrf2 activation by PQQ inhibits aging-induced IVDD by attenuating cellular senescence and matrix degradation. This study clarifies Keap1-Nrf2-Wnt5a axis as the novel signaling underlying the protective effects of PQQ against aging-related IVDD, and provides evidence for PQQ as a potential agent for clinical prevention and treatment of natural aging-induced IVDD.
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