ArticleEuropean journal of medical research2015
Beneficial reward-to-risk action of glucosamine during pathogenesis of osteoarthritis.
Article in European journal of medical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Organellophagy regulates cell death:A potential therapeutic target for inflammatory diseases.Journal of advanced research · 2025Review
- Glucosamine-loaded injectable hydrogel promotes autophagy and inhibits apoptosis after cartilage injury.Heliyon · 2023Article
- Identification of natural products and FDA-approved drugs for targeting cancer stem cell (CSC) propagation.Aging · 2022Article
- The Role of Autophagy in Osteoarthritic Cartilage.Biomolecules · 2022Review
- New insights into the interplay between autophagy and cartilage degeneration in osteoarthritis.Frontiers in cell and developmental biology · 2022Review
- The Hexosamine Biosynthetic Pathway as a Therapeutic Target after Cartilage Trauma: Modification of Chondrocyte Survival and Metabolism by Glucosamine Derivatives and PUGNAc in an Ex Vivo Model.International journal of molecular sciences · 2021Article
- Molecular docking-guided synthesis of NSAID-glucosamine bioconjugates and their evaluation as COX-1/COX-2 inhibitors with potentially reduced gastric toxicity.Chemical biology & drug design · 2021Article
- The Role of Autophagy in Osteoarthritis.Frontiers in cell and developmental biology · 2020Review
- Role of the Inflammation-Autophagy-Senescence Integrative Network in Osteoarthritis.Frontiers in physiology · 2018Review
- Erratum to: Beneficial reward-to-risk action of glucosamine during pathogenesis of osteoarthritis.European journal of medical research · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveGlucosamine is widely used to improve the symptoms and to delay the structural progression of osteoarthritis. However, its efficacy in osteoarthritis has been controversial and its underlying mechanism of action remains unclear. The aim of this study was to investigate the effects of glucosamine and the underlying mechanisms in human chondrocytes.
methodsChondrocytes from normal human articular cartilage were treated with glucosamine (10-100 mM). Subsequently, cell death was analyzed by Annexin V staining and FACS and mitochondrial function was studied by measuring the mitopotential. Peroxisomal function was analyzed by BODIPY staining, and gene expression of PMP70 and acyl-CoA oxidase 1, by real-time PCR. Total lipids were analyzed by gas chromatography/mass spectrometry. Autophagy activation was determined by western blotting of beclin and light chain 3B. Autophagosome formation was analyzed by introduction of green fluorescent protein (GFP) LC3, and pexophagy was determined by introduction of mRFP-EGFP-SKL plasmids.
resultsTreatment of chondrocytes with glucosamine exerts exposure time-dependent dual effects on apoptosis/autophagy. Short time exposure of glucosamine to chondrocytes activated autophagy, pexophagy, and peroxidation. On the other hand, long time exposure of glucosamine had opposite effects, namely accumulation of very long chain fatty acids and peroxisomal dysfunction.
conclusionWe highlight the dual role of glucosamine in apoptosis/autophagy in human chondrocytes depending on exposure time. Although further research is required to fully understand the dual effects of glucosamine, dosage and duration of glucosamine treatment are clear contributing factors towards the line of beneficial reward-to-risk action.
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