ArticleJournal of nanobiotechnology2024
Extracellular vesicles from senescent mesenchymal stromal cells are defective and cannot prevent osteoarthritis.
Article in Journal of nanobiotechnology, 2024. 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 18 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Targeting osteoarthritis with small extracellular vesicle therapy: potential and perspectives.Frontiers in bioengineering and biotechnology · 2025Pooled it
- From pathogenic to reparative: Context-Dependent function of extracellular vesicles in osteoarthritis.Bioactive materials · 2027Review
- Research progress of mesenchymal stem cells/stromal cells and their derivatives against cell senescence in the treatment of osteoarthritis.Annals of medicine · 2026Review
- Review
- Role of Collection Media on the Biological Activity of Extracellular Vesicles From hTERT-Immortalised Mesenchymal Stromal Cells.Journal of extracellular vesicles · 2026Article
- Senomorphic Small Extracellular Vesicles Delivered by a Tissue-Adhesive α-Lipoic-Acid Hydrogel Enable Immuno-Rejuvenation for Bone-Tendon Interface Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mesenchymal stem cell senescence as a potency brake: causes, consequences, and cures.Frontiers in aging · 2026Review
- Mammalian cell-derived extracellular vesicles remodel the immune-repair microenvironment in osteoarthritis: from pathological signal transmission to regenerative therapy.Frontiers in immunology · 2026Review
- From pathogenesis to therapy: extracellular vesicles in osteoarthritis.Frontiers in bioengineering and biotechnology · 2026Review
- Development of mesenchymal stem cells: therapeutic effect and prospect for rheumatoid arthritis.Stem cell research & therapy · 2025Review
- Extracellular vesicles in metabolic perspective: mechanism and targeted therapy.Journal of nanobiotechnology · 2025Review
- Ontogenetic stage and type of donor cells shape extracellular vesicles' therapeutic potential for osteoarthritis.Stem cell research & therapy · 2025Article
- Targeted Blockage of Pathological Extracellular Vesicles and Particles From Fibroblast-Like Synoviocytes for Osteoarthritis Relief: Proteomic Analysis and Cellular Effect.Journal of extracellular vesicles · 2025Article
- A bibliometric and visualized analysis of extracellular vesicles in degenerative musculoskeletal diseases (from 2006 to 2024).Frontiers in pharmacology · 2025Article
- Exosomes in cartilage microenvironment regulation and cartilage repair.Frontiers in cell and developmental biology · 2025Review
- Article
- Extracellular Vesicles: A Novel Diagnostic Tool and Potential Therapeutic Approach for Equine Osteoarthritis.Current issues in molecular biology · 2024Review
- Exosomal communication: a pivotal regulator of bone homeostasis and a potential therapeutic target.Frontiers in pharmacology · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age is the most important risk factor in degenerative diseases such as osteoarthritis (OA), which is associated with the accumulation of senescent cells in the joints. Here, we aimed to assess the impact of senescence on the therapeutic properties of extracellular vesicles (EVs) from human fat mesenchymal stromal cells (ASCs) in OA. We generated a model of DNA damage-induced senescence in ASCs using etoposide and characterized EVs isolated from their conditioned medium (CM). Senescent ASCs (S-ASCs) produced 3-fold more EVs (S-EVs) with a slightly bigger size and that contain 2-fold less total RNA. Coculture experiments showed that S-ASCs were as efficient as healthy ASCs (H-ASCs) in improving the phenotype of OA chondrocytes cultured in resting conditions but were defective when chondrocytes were proliferating. S-EVs were also impaired in their capacity to polarize synovial macrophages towards an anti-inflammatory phenotype. A differential protein cargo mainly related to inflammation and senescence was detected in S-EVs and H-EVs. Using the collagenase-induced OA model, we found that contrary to H-EVs, S-EVs could not protect mice from cartilage damage and joint calcifications, and were less efficient in protecting subchondral bone degradation. In addition, S-EVs induced a pro-catabolic and pro-inflammatory gene signature in the joints of mice shortly after injection, while H-EVs decreased hypertrophic, catabolic and inflammatory pathways. In conclusion, S-EVs are functionally impaired and cannot protect mice from developing OA.
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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 OpenQuestion graph.