ArticleJournal of cellular and molecular medicine2017
Advanced glycation end products regulate anabolic and catabolic activities via NLRP3-inflammasome activation in human nucleus pulposus cells.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.
- Extracellular Vesicles as an Emerging Treatment Option for Intervertebral Disc Degeneration: Therapeutic Potential, Translational Pathways, and Regulatory Considerations.Advanced healthcare materials · 2022Pooled it
- Itgb1-Mediated Stabilization of Vimentin Alleviates Excessive Mechanical Stress-Induced Nucleus Pulposus Cell Pyroptosis and Intervertebral Disc Degeneration via PINK1-Parkin-Dependent Mitophagy.Cell proliferation · 2026Article
- Screening of metabolic-related biomarkers linking intervertebral disc degeneration and type 2 diabetes based on comprehensive bioinformatics analysis and machine learning.Biochemistry and biophysics reports · 2026Article
- Cardiac metabolic remodeling drives dicarbonyl stress-induced mitochondrial dysfunction in experimental heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2026Article
- Adapt, Mitigate, and Target: The Role of Oxidative Stress in Intervertebral Disc Homeostasis and Disc Degeneration.Neurospine · 2026Review
- The interplay between NLRP3 inflammasome and metabolic signals in gouty arthritis.Frontiers in immunology · 2026Review
- Cellular and molecular mechanisms of diabetes-mediated disc degeneration.Frontiers in endocrinology · 2026Review
- When glycobiology meets inflammasome activation: Insights and implications.Journal of advanced research · 2026Review
- Revealing the Correlation Between NLRP3 Inflammasome-Related Genes and Intervertebral Disc Degeneration Based Multiomic Analysis and Experimental Validation.Mediators of inflammation · 2026Article
- Unraveling the causal landscape of intervertebral disc degeneration: A Mendelian randomization analysis of 108 traits.Medicine · 2025Article
- Understanding the Physiological Behavior of Disc Cells in an In Vitro Imitation of the Healthy and Degenerated Disc Niche.JOR spine · 2025Article
- Mechanistic Insight into Phenolic Compounds in Mitigating Diabetic Complications Induced by Advanced Glycation End Products.Current issues in molecular biology · 2025Review
- Article
- Pyroptosis: A spoiler of peaceful coexistence between cells in degenerative bone and joint diseases.Journal of advanced research · 2025Review
- Integrated bulk and single-cell RNA sequencing to identify potential biomarkers in intervertebral disc degeneration.European journal of medical research · 2025Article
- Targeting advanced glycation end products: potential therapeutic approaches for mitigating diabetic intervertebral disc degeneration?Frontiers in endocrinology · 2025Review
- Mechanisms of AGE-induced VSMC phenotypic switching and macrophage modulation in human abdominal aortic aneurysms.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Gubi Decoction Ameliorates Porous Cartilage Endplate in an Intervertebral Disc Degeneration Model Mouse Through Inhibition of NF-κB Activity and Pyroptosis.Journal of inflammation research · 2025Article
- Region-specific mitophagy in nucleus pulposus, annulus fibrosus, and cartilage endplate of intervertebral disc degeneration: mechanisms and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Melatonin mitigates intervertebral disc degeneration by suppressing NLRP3 inflammasome activation via the EGR1/DDX3X pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration is widely recognized as a cause of lower back pain, neurological dysfunction and other musculoskeletal disorders. The major inflammatory cytokine IL-1β is associated with intervertebral disc degeneration; however, the molecular mechanisms that drive IL-1β production in the intervertebral disc, especially in nucleus pulposus (NP) cells, are unknown. In some tissues, advanced glycation end products (AGEs), which accumulate in NP tissues and promote its degeneration, increase oxidative stress and IL-1β secretion, resulting in disorders, such as obesity, diabetes mellitus and ageing. It remains unclear whether AGEs exhibit similar effects in NP cells. In this study, we observed significant activation of the NLRP3 inflammasome in NP tissues obtained from patients with degenerative disc disease compared to that with idiopathic scoliosis according to results detected by Western blot and immunofluorescence. Using NP cells established from healthy tissues, our in vitro study revealed that AGEs induced an inflammatory response in NP cells and a degenerative phenotype in a NLRP3-inflammasome-dependent manner related to the receptor for AGEs (RAGE)/NF-κB pathway and mitochondrial damage induced by mitochondrial reactive oxygen species (mtROS) generation, mitochondrial permeability transition pore (mPTP) activation and calcium mobilization. Among these signals, both RAGE and mitochondrial damage primed NLRP3 and pro-IL-1β activation as upstream signals of NF-κB activity, whereas mitochondrial damage was critical for the assembly of inflammasome components. These results revealed that accumulation of AGEs in NP tissue may initiate inflammation-related degeneration of the intervertebral disc via activation of the NLRP3 inflammasome.
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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.