ArticleNutrients2022
Friedelin Alleviates the Pathogenesis of Collagenase-Induced Tendinopathy in Mice by Promoting the Selective Autophagic Degradation of p65.
Article in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Friedelin Enhances Gelatin/Nanohydroxyapatite Scaffold Performance by Inhibiting Osteoclastogenesis and Promoting Osteogenesis.ACS omega · 2026Article
- Friedelin Ameliorates Nucleus Pulposus Inflammation by Increasing p65 Autophagic Degradation to Inhibit NF-κB Signalling Pathway.Journal of cellular and molecular medicine · 2026Article
- Friedelin: A natural compound exhibited potent antibacterial, anti-inflammatory, and wound healing properties against MRSA-infected wounds.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Immunoinflammation and post-translational modifications in the aging process.Journal of translational medicine · 2025Review
- Article
- Malvidin attenuates trauma-induced heterotopic ossification of tendon in rats by targeting Rheb for degradation via the ubiquitin-proteasome pathway.Journal of cellular and molecular medicine · 2024Article
- Establishment of a Mouse Degenerative Model of Patellar Tendinopathy with Upregulation of Inflammation.International journal of molecular sciences · 2024Article
- The roles and mechanisms of the NF-κB signaling pathway in tendon disorders.Frontiers in veterinary science · 2024Review
- Pristimerin suppresses AIM2 inflammasome by modulating AIM2-PYCARD/ASC stability via selective autophagy to alleviate tendinopathy.Autophagy · 2024Article
- Animal model for tendinopathy.Journal of orthopaedic translation · 2023Review
- Inhibition of RNF182 mediated by Bap promotes non-small cell lung cancer progression.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
With the development of an aging population, tendinopathy has become a common musculoskeletal disease in the elderly with a high recurrence rate and no curative treatment. The inflammation mediated by NF-κB signaling plays an important role in tendon senescence and degeneration. Friedelin (FR) is a triterpenoid derived from green plants, which has a variety of pharmacological functions, such as analgesia, anti-inflammation, antioxidation, and anti-tumor functions. However, the role and mechanism of FR in tendinopathy are unclear. Here, we found that FR improved the mechanical strength of the Achilles tendon, restored the orderly arrangement of collagen fibers, reduced inflammatory cell infiltration, and promoted tenogenesis, thereby blocking the progression of tendinopathy. Mechanistically, FR promoted the autophagic degradation of p65 by enhancing the interaction between p62 and p65 and effectively inhibited the activation of the NF-κB pathway, thus alleviating the inflammatory response of tenocytes. In addition, FR recruited E3 ubiquitin enzyme RNF182 to increase the K48-linked ubiquitination of p65 and promoted p62-mediated autophagic degradation. Furthermore, blocking ubiquitination reversed the degradation of p65 by FR. Therefore, these findings identify the new pharmacological mechanism of the anti-inflammatory effect of FR and provide a new candidate drug for the treatment of tendinopathy.
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Registered trials
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