ReviewRegenerative therapy2022
Hypoxia inducible factor-1α mediates the mechanism of the Hedgehog pathway in tendinopathy repair by Asperosaponin VI.
Review in Regenerative therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
4 citing papers in PubMed, 4 citations in OpenAlex.
- Recent advances in tendon redox biology: the interplay of oxidative stress, calcium signaling, and antioxidant defence mechanisms.Frontiers in pharmacology · 2026Review
- Simultaneous detection of multiple mycotoxins in Radix Dipsaci and estimation of exposure risk for consumers.Scientific reports · 2024Article
- Hypoxia-Inducible Factor and Oxidative Stress in Tendon Degeneration: A Molecular Perspective.Antioxidants (Basel, Switzerland) · 2024Review
- Drug Delivery Approaches to Improve Tendon Healing.Tissue engineering. Part B, Reviews · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Our previous study found that asperosaponin VI (ASA VI) has a positive effect on the repair of tendinopathy. However, its molecular biological mechanism is unclear. Objective: To investigate the role of hypoxia inducible factor-1α (HIF-1α) in mediating the hedgehog (Hh) pathway in tendinopathy repair by ASA VI. Methods: A total of 36 2-month-old female SD rats were classified into the normal group (NG, n = 10) and tendinopathy model group (n = 26). The tendinopathy model group was further divided into the model group (MG), ASA VI group (AG), and triamcinolone acetonide + lidocaine group (TG). Results: Compared with those in the MG group, IL-1 mRNA was significantly downregulated and IL-4 and IL-10 were increased in the AG group (P < 0.01). The mRNA expression levels of MMP3, TIMP3, VEGF-A, KDR, and VWF mRNA decreased (P < 0.01). Immunofluorescence staining revealed that CD31/endomucin levels were significantly attenuated. Scx, Mkx, EYA1, EYA2, COL1, COL3, and TNC mRNA levels showed significant differences (P < 0.01). Immunofluorescence staining suggested the upregulation of Scx and the downregulation of Sox9. Shh, Ptch1, Smo, Gli1, Cyc-D1, Cyc-E1, and c-Myc mRNA levels were downregulated (P < 0.01). The protein expression levels of Gli 1, Shh, and Ptch1 decreased significantly (P < 0.01). The immunofluorescence staining levels of Shh, Ptch, and Gli 1 significantly decreased. Conclusion: ASA VI inhibits local vascular hyperproliferation and downregulates the HIF-1α/Hh pathway to promote the tendinous differentiation of tendon stem/progenitor cells and the repair of tendinopathy. The effect of ASA VI on HIF-1α levels may be an effective target in the treatment of tendinopathy.
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