ArticleArthritis and rheumatism2010
Autophagy is a protective mechanism in normal cartilage, and its aging-related loss is linked with cell death and osteoarthritis.
Article in Arthritis and rheumatism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 378 papers, 2 of them syntheses that pooled it.
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Who cites it
378 citing papers in PubMed, 2 syntheses or guidelines pooled it, 623 citations in OpenAlex.
- Pooled it
- Knowledge mapping of autophagy in osteoarthritis from 2004 to 2022: A bibliometric analysis.Frontiers in immunology · 2023Pooled it
- Molecular hydrogen and osteoarthritis: multi-target mechanisms and therapeutic effectiveness.Medical gas research · 2027Review
- The Anti-Osteoarthritis Effect of Medicinal and Edible Homologous Bioactive Components and Chinese Medicinal and Health Food Varieties.Nutrients · 2026Review
- Engineered Injectable Hydrogel Platform for Tailoring the Osteoarthritis Microenvironment.Advanced healthcare materials · 2026Review
- From Joint Loading to Osteoarthritis: A Multiscale Review of Knee Mechanobiology and Digital Modelling.International journal of molecular sciences · 2026Review
- Article
- Polygonatum sibiricum polysaccharides regulate chondrocyte inflammation and metabolism via S100A9 inhibition-mediated autophagy promotion to ameliorate osteoarthritis.BMC complementary medicine and therapies · 2026Article
- Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Crosstalk between autophagy and ferroptosis related genes in osteoarthritis: insights from transcriptomic and in vitro analyses.Irish journal of medical science · 2026Article
- Empagliflozin Alleviates Osteoarthritis Progression by Attenuating Inflammation, Restoring Impaired Autophagy, and Ameliorating Chondrocyte Senescence.Biomedicines · 2026Article
- Plasma Proteomics Reveals Persistent and Surgery-Responsive Molecular Signatures in Osteoarthritis Patients.International journal of molecular sciences · 2026Article
- M1 macrophage-derived migrasomes ameliorate temporomandibular joint osteoarthritis via autophagy.Journal of nanobiotechnology · 2026Article
- The osteoarthritis inflammatory ecosystem: a node-edge-boundary-emergent framework toward precision stratification and therapeutic hypothesis generation.Frontiers in medicine · 2026Review
- Pain Modulation, Inflammation-Regulatory Mechanisms, and Translational Boundaries of Evidence for Acupuncture-Related Therapies in Knee Osteoarthritis: A Structured Narrative Review.Journal of pain research · 2026Review
- The dual role of autophagy in cartilage degradation: from mechanisms to targeted therapeutics.Frontiers in cell and developmental biology · 2026Review
- Propionate attenuates osteoarthritis progression by regulating the gut-joint axis.Frontiers in immunology · 2026Article
- Increased Rab1a accelerates osteoarthritis by inhibiting autophagy via activation of the mTORC1-S6K pathway.Journal of advanced research · 2025Article
- Article
318 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveAutophagy is a process for turnover of intracellular organelles and molecules that protects cells during stress responses. We undertook this study to evaluate the potential roles of Unc-51-like kinase 1 (ULK1), an inducer of autophagy, Beclin1, a regulator of autophagy, and microtubule-associated protein 1 light chain 3 (LC3), which executes autophagy, in the development of osteoarthritis (OA) and in cartilage cell death.
methodsExpression of ULK1, Beclin1, and LC3 was analyzed in normal and OA human articular cartilage and in knee joints of mice with aging-related and surgically induced OA, using immunohistochemistry and Western blotting. Poly(ADP-ribose) polymerase (PARP) p85 expression was used to determine the correlation between cell death and autophagy.
resultsULK1, Beclin1, and LC3 were constitutively expressed in normal human articular cartilage. ULK1, Beclin1, and LC3 protein expression was reduced in OA chondrocytes and cartilage, but these 3 proteins were strongly expressed in the OA cell clusters. In mouse knee joints, loss of glycosaminoglycans (GAGs) was observed at ages 9 months and 12 months and in the surgical OA model, 8 weeks after knee destabilization. Expression of ULK1, Beclin1, and LC3 decreased together with GAG loss, while PARP p85 expression was increased.
conclusionAutophagy may be a protective or homeostatic mechanism in normal cartilage. In contrast, human OA and aging-related and surgically induced OA in mice are associated with a reduction and loss of ULK1, Beclin1, and LC3 expression and a related increase in apoptosis. These results suggest that compromised autophagy represents a novel mechanism in the development of OA.
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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.