ArticleActa pharmaceutica Sinica. B2025
Extracellular vesicles deliver thioredoxin to rescue stem cells from senescence and intervertebral disc degeneration
Article in Acta pharmaceutica Sinica. B, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Antioxidant Nanotherapies for Intervertebral Disk Degeneration: Progress and Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Clinical Applications of Extracellular Vesicles: Promises and Pitfalls.International journal of molecular sciences · 2026Review
- PACS-2 Mitigates NPSC Apoptosis and Intervertebral Disc Degeneration by Preserving MAM Integrity via the SP1/LRRK2/Mfn2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Oxidative Stress as a Central Mechanistic Bridge Between Alzheimer's and Vascular Pathologies in Mixed Dementia: Emerging Evidence and Therapeutic Perspectives.Biomedicines · 2025Article
- The Role of Extracellular Vesicles in Musculoskeletal Diseases.Journal of extracellular vesicles · 2025Review
- The Redox Enzyme Thioredoxin Is Increased in Plasma Extracellular Vesicles From Endurance-Trained Females in Response to Acute Exercise.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Roles of exosomes in immune regulation of osteoarthritis and their applications in inflammation repair.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) is largely attributed to impaired endogenous repair. Nucleus pulposus-derived stem cells (NPSCs) senescence leads to endogenous repair failure. Small extracellular vesicles/exosomes derived from mesenchymal stem cells (mExo) have shown great therapeutic potential in IDD, while whether mExo could alleviate NPSCs senescence and its mechanisms remained unknown. We established a compression-induced NPSCs senescence model and rat IDD models to evaluate the therapeutic efficiency of mExo and investigate the mechanisms. We found that mExo significantly alleviated NPSCs senescence and promoted disc regeneration while knocking down thioredoxin (TXN) impaired the protective effects of mExo. TXN was bound to various endosomal sorting complex required for transport (ESCRT) proteins. Autocrine motility factor receptor (AMFR) mediated TXN K63 ubiquitination to promote the binding of TXN on ESCRT proteins and sorting of TXN into mExo. Knocking down exosomal TXN inhibited the transcriptional activity of nuclear factor erythroid 2-related factor 2 (NRF2) and activator protein 1 (AP-1). NRF2 and AP-1 inhibition reduced endogenous TXN production that was promoted by exosomal TXN. Inhibition of NRF2
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Registered trials
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