ArticleCell cycle (Georgetown, Tex.)2022
Mesenchymal stem cell-derived exosome mediated long non-coding RNA KLF3-AS1 represses autophagy and apoptosis of chondrocytes in osteoarthritis.
Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 47 citations in OpenAlex.
- Mesenchymal stromal cells therapy for remodeling the joint microenvironment: mechanisms, nanotechnology-enhanced strategies, and translation prospects.Stem cell research & therapy · 2026Review
- Exosomes in Alzheimer's disease: neuroinflammation mitigation via immune modulation and inflammatory pathway targeting.Molecular biology reports · 2026Review
- Engineered exosome biomedical technologies for precision diagnosis and therapy in orthopedic diseases.Frontiers in medicine · 2026Review
- Exercise stress and tissue remodeling: advances in exosome-mediated RNA-RBP networks in musculoskeletal injury repair and functional recovery.Frontiers in genetics · 2026Review
- The dual role of autophagy in cartilage degradation: from mechanisms to targeted therapeutics.Frontiers in cell and developmental biology · 2026Review
- Multiple strategies, one mission: mesenchymal stromal cell-based mechanisms of action in osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Mammalian cell-derived extracellular vesicles remodel the immune-repair microenvironment in osteoarthritis: from pathological signal transmission to regenerative therapy.Frontiers in immunology · 2026Review
- The crosstalk among macrophages, chondrocytes and mesenchymal stem cells in osteoarthritis: the role of extracellular vesicles.Stem cell research & therapy · 2025Review
- Osteoarthritis: Mechanisms and Therapeutic Advances.MedComm · 2025Review
- Unveiling the potential of MSC extracellular vesicles: MiR-122-5p enhancing chondrocyte regeneration in osteoarthritis via autophagy mechanism.Stem cell research & therapy · 2025Article
- PDGF-BB promotes oral submucosal fibrosis by driving phenotypic transformation and autophagy in oral mucosal fibroblasts through downregulation of circHIPK3.Scientific reports · 2025Article
- Progress in multi-omics studies of osteoarthritis.Biomarker research · 2025Review
- BMSC Derived Exosomes Attenuate Apoptosis of Temporomandibular Joint Disc Chondrocytes in TMJOA via PI3K/AKT Pathway.Stem cell reviews and reports · 2025Article
- Exosomal non-coding RNAs in the regulation of bone metabolism homeostasis: Molecular mechanism and therapeutic potential.Heliyon · 2025Review
- Mechanism of cell death and its application in the repair of inflammatory bowel disease by mesenchymal stem cells.Frontiers in immunology · 2025Review
- Non-coding RNA in cartilage regeneration: regulatory mechanism and therapeutic strategies.Frontiers in bioengineering and biotechnology · 2025Review
- Exosomes in cartilage microenvironment regulation and cartilage repair.Frontiers in cell and developmental biology · 2025Review
- Regulating the regulators: long non-coding RNAs as autophagic controllers in chronic disease management.Journal of biomedical science · 2024Review
- Mapping the knowledge landscape: A bibliometric analysis of exosome research in osteoarthritis (2004-2023).Heliyon · 2024Review
- MSC Promotes the Secretion of Exosomal lncRNA KLF3-AS1 to Regulate Sphk1 Through YY1-Musashi-1 Axis and Improve Cerebral Ischemia-Reperfusion Injury.Molecular neurobiology · 2024Article
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Authors and funding
5 authors.
Funding
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Abstract
Osteoarthritis is a degenerative joint disease and a leading cause of adult disability. Our previous study has reported that mesenchymal stem cell-derived exosomes (MSC-Exo) mediated long non-coding RNA KLF3-AS1 improves osteoarthritis. This study aims to investigate the molecular mechanism of KLF3-AS1 in osteoarthritis. Chondrocytes were treated with IL-1β to induce chondrocyte injury, followed by MSC-Exo treatment. We found that MSC-Exo enhanced KLF3-AS1 expression in IL-1β-treated chondrocytes. IL-1β treatment reduced cell viability and enhanced apoptosis in chondrocytes. MSC-Exo-mediated KLF3-AS1 promoted cell viability and repressed apoptosis of IL-1β-treated chondrocytes. Rapamycin (autophagy activator) promoted cell viability and suppressed apoptosis of chondrocytes by activating autophagy. Moreover, KLF3-AS1 interacted with YBX1 in chondrocytes. MSC-Exo-mediated KLF3-AS1 activated PI3K/Akt/mTOR signaling pathway, which was abrogated by YBX1 silencing. MSC-Exo-mediated KLF3-AS1 repressed autophagy and apoptosis of chondrocytes by activating PI3K/Akt/mTOR signaling pathway. In conclusion, our data demonstrate that MSC-Exo-mediated KLF3-AS1 inhibits autophagy and apoptosis of IL-1β-treated chondrocyte through PI3K/Akt/mTOR signaling pathway. KLF3-AS1 activates PI3K/Akt/mTOR signaling pathway by targeting YBX1 to improve the progression of osteoarthritis. Thus, this work suggests that MSC-Exo-mediated KLF3-AS1 may be a potential therapeutic target for osteoarthritis.
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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 Socratic graph.