ArticleCell death & disease2020
AQP1 modulates tendon stem/progenitor cells senescence during tendon aging.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 79 citations in OpenAlex.
- Quercetin attenuates tendon stem/progenitor cell senescence and promotes aged tendon repair via AKT/NF-κB/NLRP3-mediated mitophagy activation.Journal of advanced research · 2026Article
- Beyond local injury: pathogenic roles of metabolic, endocrine, and aging-associated systemic factors in tendinopathy and novel therapeutic strategies.Journal of orthopaedic surgery and research · 2026Review
- Aquaporin-1 stabilizes β-catenin to promote NLRP3 inflammasome-mediated pyroptosis in rheumatoid arthritis.Apoptosis : an international journal on programmed cell death · 2026Article
- Stability of non-canonical nucleic acid structure as a potential modulator of cell fate.Nucleic acids research · 2026Review
- The HMGB1/RAGE/β-catenin axis mediates aberrant osteogenic-tenogenic differentiation imbalance of tendon stem/progenitor cells in diabetic tendinopathy.Journal of orthopaedic surgery and research · 2025Article
- Aquaporin-1 Facilitates Macrophage M1 Polarization by Enhancing Glycolysis Through the Activation of HIF1α in Lipopolysaccharide-Induced Acute Kidney Injury.Inflammation · 2025Article
- Tendon Aging: A Silent Enemy Revealed Strategies for Effective Treatment.Aging medicine (Milton (N.S.W)) · 2025Review
- Stem cell-derived exosomes: a potential therapeutic strategy for enhancing tendon stem/progenitor cells function in tendon-bone healing.Journal of orthopaedic surgery and research · 2025Review
- Immunosenescence in Sepsis: Molecular Mechanisms and Potential Therapeutic Targets.Aging and disease · 2025Review
- Erroneous Differentiation of Tendon Stem/Progenitor Cells in the Pathogenesis of Tendinopathy: Current Evidence and Future Perspectives.Stem cell reviews and reports · 2025Review
- Tendon Tissue Engineering: Pathophysiological Mechanism and Bioengineering Therapy of Tendinopathy.International journal of nanomedicine · 2025Review
- Cellular senescence impairs tendon extracellular matrix remodeling in response to mechanical unloading.Aging cell · 2024Article
- HMGB1 Modulates High Glucose-Induced Erroneous Differentiation of Tendon Stem/Progenitor Cells through RAGE/Stem cells international · 2024Article
- Effect of Aging on Tendon Biology, Biomechanics and Implications for Treatment Approaches.International journal of molecular sciences · 2023Review
- Aquaporin 1 Facilitates Ferroptosis, M1 Polarization, Mitochondrial Dysfunction, and Autophagy Damage on Lipopolysaccharide-Induced Macrophage Through Down-Regulation of P53 Signaling Pathway.DNA and cell biology · 2023Article
- The Regulation of the AMPK/mTOR Axis Mitigates Tendon Stem/Progenitor Cell Senescence and Delays Tendon Aging.Stem cell reviews and reports · 2023Article
- Biomimetic Scaffolds for Tendon Tissue Regeneration.Biomimetics (Basel, Switzerland) · 2023Review
- Saikosaponin d (SSD) alleviates diabetic peripheral neuropathy by regulating the AQP1/RhoA/ROCK signaling in streptozotocin-induced diabetic rats.Acta diabetologica · 2023Article
- Targeting Senescent Tendon Stem/Progenitor Cells to Prevent or Treat Age-Related Tendon Disorders.Stem cell reviews and reports · 2023Review
- Parishin A-loaded mesoporous silica nanoparticles modulate macrophage polarization to attenuate tendinopathy.NPJ Regenerative medicine · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The link between tendon stem/progenitor cells (TSPCs) senescence and tendon aging has been well recognized. However, the cellular and molecular mechanisms of TSPCs senescence are still not fully understood. In present study, we investigated the role of Aquaporin 1 (AQP1) in TSPCs senescence. We showed that AQP1 expression declines with age during tendon aging. In aged TSPCs, overexpression of AQP1 significantly attenuated TSPCs senescence. In addition, AQP1 overexpression also restored the age-related dysfunction of self-renewal, migration and tenogenic differentiation. Furthermore, we demonstrated that the JAK-STAT signaling pathway is activated in aged TSPCs, and AQP1 overexpression inhibited the JAK-STAT signaling pathway activation which indicated that AQP1 attenuates senescence and age-related dysfunction of TSPCs through the repression of JAK-STAT signaling pathway. Taken together, our findings demonstrated the critical role of AQP1 in the regulation of TSPCs senescence and provided a novel target for antagonizing tendon aging.
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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.