ArticleStem cell reviews and reports2025
HMGA2 Attenuates Tendon Stem/Progenitor Cell Senescence Via PI3K/AKT-Mediated Mitophagy Activation and SASP Suppression.
Article in Stem cell reviews and reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- 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
- Phenotypic alterations and PI3K-AKT pathway regulation in senescence of human tonsil mesenchymal stem cells.Stem cell research & therapy · 2026Article
- ROS-responsive hydrogel loaded with capsaicin promotes tenogenic differentiation of tendon stem/progenitor cells and enhances tendon injury repair.Materials today. Bio · 2026Article
- 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
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Authors and funding
11 authors.
Funding
Abstract
Tendon stem/progenitor cell (TSPC) senescence contributes to age-related tendon degeneration, yet the molecular mechanisms underlying this process remain poorly understood. In present study, we investigated the role of High-Mobility Group A2 (HMGA2) in TSPCs senescence. During the tendon aging, we showed that HMGA2 expression decreases with age. In senescent TSPCs, HMGA2 overexpression significantly delayed TSPCs senescence. Additionally, overexpression of HMGA2 restored the age-related dysfunction of migration, tenogenic differentiation, and mitophagy. HMGA2 also suppressed the senescence-associated secretory phenotype (SASP), downregulating inflammatory cytokines such as IL-1β, IL-6, and TGF-β. Furthermore, we suggested that the PI3K-AKT signaling pathway is activated in senescent TSPCs, and HMGA2 overexpression could inhibit the PI3K-AKT signaling pathway activation, which demonstrates that HMGA2 might attenuate senescence and age-related dysfunction of TSPCs through the repression of PI3K-AKT signaling pathway. Our findings collectively indicated the crucial involvement of HMGA2 in TSPCs senescence regulation and suggested a novel target for preventing tendon aging.
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Registered trials
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