ArticleJournal of cachexia, sarcopenia and muscle2025
Atrophy Masseter Recovery by Electrical Stimulation Mediated M2-Like Macrophage Polarisation via JAK/PI3K/AKT Pathway.
Article in Journal of cachexia, sarcopenia and muscle, 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.
- Engineered piezoelectric dressings advance cutaneous wound healing.Bioactive materials · 2026Review
- Metrnl and macrophage polarization: role in skeletal muscle homeostasis and therapeutic potential.Frontiers in immunology · 2026Review
- Translating physical stress into biological signals: precision electro-oncology based on conformational changes of electro-sensitive receptors and parameterized immune remodeling.Frontiers in oncology · 2026Review
- The role of macrophage polarization in organ transplantation: research progress on impact on graft injury, repair, and fibrosis.Frontiers in immunology · 2026Review
- Atrophy Masseter Recovery by Electrical Stimulation Mediated M2-Like Macrophage Polarisation via JAK/PI3K/AKT Pathway.Journal of cachexia, sarcopenia and muscle · 2025Article
- Electrospinning for Mimicking Bioelectric Microenvironment in Tissue Regeneration.Research (Washington, D.C.) · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
backgroundAtrophy of the masseter muscle can result in an aged facial appearance and diminished chewing function. Electrical stimulation (ES) is known for its ability to facilitate tissue healing and functional recovery, but its precise role in the repair of atrophic masseter muscles remains incompletely understood.
methodsWe induced masseter muscle atrophy in rats through botulinum toxin (BTX) injection and subsequently treated the animals with or without ES. Single-nucleus sequencing (sn-RNA seq) was conducted to analyse the changes in macrophages of masseter muscles between control, BTX and BTX + ES groups. The role and mechanism of macrophage phenotypic transformation in the process of ES promoting the recovery of atrophied masseter muscles were both verified through in vivo and in vitro experiments.
resultsOur results indicate that ES treatment within defined current parameters significantly ameliorated muscle condition by reducing atrophy-related gene expression (MuRF1: BTX: 10.15 ± 1.69; BTX + ES: 1.05 ± 0.06; Fbxo32: BTX: 8.62 ± 1.19, BTX + ES: 1.19 ± 0.07, p < 0.0001) and enhancing vascularisation (Vegf positive area: BTX: 6.60 ± 2.87%, BTX + ES: 27.23 ± 1.70%, p < 0.001). Analysis conducted with sn-RNA seq demonstrated increased infiltration of M1 macrophages during muscle atrophy, with a subsequent transition to M2 macrophages following ES treatment (M1 macrophage portion: Ctrl: 15.2%, BTX: 25.8%, BTX + ES: 14.7%; M2 macrophages: Ctrl: 67.9%, BTX: 46.9%, BTX + ES: 70.5%). Further investigations demonstrated that ES reduced M1 macrophage infiltration (five-fold lower of CD86
conclusionsOur findings suggest that ES can enhance masseter muscle tissue repair by modulating macrophage polarisation, offering valuable insights into the potential of ES in noninvasive tissue regeneration strategies for treating masseter muscle atrophy.
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