ArticleStem cell research & therapy2025
Puerarin relives inflammation, bone destruction and facilitates osteogenic differentiation in periodontitis by enhancing mitochondrial autophagy via activating mitochondrial Mitofusin 2.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Puerarin alleviates inflammation and promotes osteogenic differentiation in periodontitis: insights from autophagy and Notch signaling pathway.Odontology · 2026Article
- Traditional Chinese medicine-derived monomers improve bone metabolic imbalance and delay osteoporosis progression by regulating mitochondrial homeostasis.Frontiers in cell and developmental biology · 2026Review
- Molecular Mechanisms and Therapeutic Potential of Puerariae Lobatae Radix in Bone Metabolism: A Comprehensive Review.Drug design, development and therapy · 2026Review
- Periodontitis Phenotypes and Treatment Outcomes Following Combined Periodontal and Orthodontic Therapy: A Cohort Study.Clinical, cosmetic and investigational dentistry · 2026Article
- Ultra-small coordination dihydromyricetin nanodots attenuate alveolar bone resorption in periodontitis through inhibition of ITGB3-Driven osteoclast differentiation.Materials today. Bio · 2025Article
- An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions.Cellular and molecular life sciences : CMLS · 2025Review
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9 authors.
Funding
Abstract
purposePuerarin (Pue) has recently been reported to have therapeutic effects on periodontitis (PD). However, there is insufficient evidence, and the mechanism involved has not yet been revealed. This work delved to explore the exact therapeutic effects and molecular mechanism of Pue in treating PD.
methodsPD mouse (C57BL/6 N mouse) model constructed by Porphyromonas gingivalis-lipopolysaccharide (Pg-LPS) induction was treated with Pue. Therapeutic efficacy of Pue for PD was examined by a series of experiments. PD cell model was induced by treating human periodontal ligament cells with Pg-LPS. Therapeutic effects of Pue on PD cell model, along with the potential molecular mechanism, were explored by logical experiments. Rescue experiments based on in vitro and in vivo studies were implemented to validate the molecular mechanism of Pue in treating PD.
resultsIn PD mice, Pue treatment relieved inflammation and bone destruction, facilitated osteogenic differentiation and autophagy in periapical tissues. In PD cell model, Pue treatment facilitated osteogenic differentiation and mitochondrial autophagy; suppressed inflammation and mitochondrial reactive oxygen species; maintained mitochondrial membrane potential and mitochondrial kinetic homeostasis; and activated mitochondrial Mitofusin 2 (Mfn2). However, these influences of Pue on PD cell model were eliminated by CsA (mitochondrial autophagy inhibitor). The enhanced mitochondrial autophagy induced by Pue was reversed by Mfn2 silencing. Through in vivo data, Mfn2 knockdown counteracted the therapeutic effects of Pue on PD mice.
conclusionPue exerted therapeutic effects on PD, possibly by enhancing mitochondrial autophagy via activating mitochondrial Mfn2. This might be a cure for PD.
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