ArticleArthritis and rheumatism2013
Glucosamine activates autophagy in vitro and in vivo.
Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 94 citations in OpenAlex.
- Glucosamine Promotes Autophagy and Attenuates Hepatic Steatosis Via O-GlcNAcylation-Mediated Mechanisms.Journal of biochemical and molecular toxicology · 2026Article
- Targeting Liquid-Liquid Phase Separation and Autophagy in Alzheimer's Disease: Insights into Molecular Mechanisms and Therapeutic Potential.Neurochemical research · 2025Review
- Neuroprotective Effects of Glucosamine in Huntington's Disease Through NLRP3 Inflammasome Inhibition.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Forkhead box O proteins in chondrocyte aging and diseases.Journal of orthopaedic translation · 2025Review
- Metabolic Reprogramming in Stromal and Immune Cells in Rheumatoid Arthritis and Osteoarthritis: Therapeutic Possibilities.European journal of immunology · 2025Review
- The role of FoxO3a in the pathogenesis of osteoarthritis and its therapeutic applications.Frontiers in immunology · 2025Review
- Autophagy in Osteoarthritis: A Double-Edged Sword in Cartilage Aging and Mechanical Stress Response: A Systematic Review.Journal of clinical medicine · 2024Review
- Association between genetically proxied glucosamine and risk of cancer and non-neoplastic disease: A Mendelian randomization study.Frontiers in genetics · 2024Article
- Ethanolic Extract of Propolis Modulates Autophagy-Related microRNAs in Osteoarthritic Chondrocytes.International journal of molecular sciences · 2023Article
- The Role of Autophagy in Osteoarthritic Cartilage.Biomolecules · 2022Review
- Cyclic mechanical strain with high-tensile triggers autophagy in growth plate chondrocytes.Journal of orthopaedic surgery and research · 2022Article
- New insights into the interplay between autophagy and cartilage degeneration in osteoarthritis.Frontiers in cell and developmental biology · 2022Review
- Autophagy and Polyphenols in Osteoarthritis: A Focus on Epigenetic Regulation.International journal of molecular sciences · 2021Review
- 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
- CREB Ameliorates Osteoarthritis Progression Through Regulating Chondrocytes AutophagyFrontiers in cell and developmental biology · 2021Article
- Histological Evaluation and Gene Expression Profiling of Autophagy-Related Genes for Cartilage of Young and Senescent Rats.International journal of molecular sciences · 2020Article
- Article
- Mitochondria: Potential Targets for Osteoarthritis.Frontiers in medicine · 2020Review
- [Role of autophagy in the pathogenesis of periodontitis].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2019Review
- Propolis Reduces the Expression of Autophagy-Related Proteins in Chondrocytes under Interleukin-1β Stimulus.International journal of molecular sciences · 2019Article
Corrections and comments
- Commented on by
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveAging-associated changes in articular cartilage represent a main risk factor for osteoarthritis (OA). Autophagy is an essential cellular homeostasis mechanism. Aging-associated or experimentally induced defects in autophagy contribute to organismal- and tissue-specific aging, while enhancement of autophagy may protect against certain aging-related pathologies such as OA. The objective of this study was to determine whether glucosamine can activate autophagy.
methodsChondrocytes from normal human articular cartilage were treated with glucosamine (0.1- 10 mM). Autophagy activation and phosphorylation levels of Akt, FoxO3, and ribosomal protein S6 were determined by Western blotting. Autophagosome formation was analyzed by confocal microscopy. Reporter mice systemically expressing green fluorescent protein (GFP) fused to light chain 3 (LC3) (GFP-LC3-transgenic mice) were used to assess changes in autophagy in response to starvation and glucosamine treatment.
resultsGlucosamine treatment of chondrocytes activated autophagy, as indicated by increased LC3-II levels, formation of LC3 puncta, and increased LC3 turnover. This was associated with glucosamine-mediated inhibition of the Akt/FoxO3/mammalian target of rapamycin pathway. Administration of glucosamine to GFP-LC3-transgenic mice markedly activated autophagy in articular cartilage.
conclusionGlucosamine modulates molecular targets of the autophagy pathway in vitro and in vivo, and the enhancement of autophagy is mainly dependent on the Akt/FoxO/mTOR pathway. These findings suggest that glucosamine is an effective autophagy activator and should motivate future studies on the efficacy of glucosamine in modifying aging-related cellular changes and supporting joint health.
Indexed as
Identifiers
What OpenQuestion holds
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.