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<p>Denervation induces severe muscle atrophy characterized by inflammatory responses and tissue degradation, with limited effective therapeutic options. This study investigates the role of the α7 nicotinic acetylcholine receptor (α7nAChR) in denervation-induced muscle atrophy and evaluates electroacupuncture (EA) as a potential treatment strategy. Using a sciatic nerve transection mouse model, we observe that denervation decreases α7nAChR expression, activates proteolytic pathways. We find that α7nAChR degradation is associated with the activation of inflammatory cytokines and the caspase pathway. In α7nAChR knockout mice, we demonstrate that α7nAChR modulates mitochondrial metabolism and fiber-type composition. It exerts protective effects by activating the AKT-FOXO1 pathway, thereby reducing inflammation and apoptosis, processes that are critical for muscle regeneration. Additionally, treatment with PNU120596 or EA restores α7nAChR function and alleviates muscle atrophy. Our findings suggest that targeting α7nAChR offers a promising therapeutic approach for muscle wasting following denervation, with potential implications for clinical management and future intervention strategies.</p>

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Activation of α7nAChR reduces inflammation and apoptosis, promoting muscle regeneration through the AKT-FOXO1 pathway

  • 期刊论文

  • 发表日期：

    2026年4月3日

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  • Xiaolu Jin,
  • Ya Zhou,
  • Luning Sun,
  • Li Li,
  • Chaozhu Zheng,
  • Zhongliang Shan,
  • Chao Ding,
  • Dongdong Huang,
  • Qipeng Zhang,
  • Rongrong Fan,
  • Guan Sun,
  • Meihong Shen,
  • Hongwei Wang,
  • Zhiqiang Huang

摘要

Denervation induces severe muscle atrophy characterized by inflammatory responses and tissue degradation, with limited effective therapeutic options. This study investigates the role of the α7 nicotinic acetylcholine receptor (α7nAChR) in denervation-induced muscle atrophy and evaluates electroacupuncture (EA) as a potential treatment strategy. Using a sciatic nerve transection mouse model, we observe that denervation decreases α7nAChR expression, activates proteolytic pathways. We find that α7nAChR degradation is associated with the activation of inflammatory cytokines and the caspase pathway. In α7nAChR knockout mice, we demonstrate that α7nAChR modulates mitochondrial metabolism and fiber-type composition. It exerts protective effects by activating the AKT-FOXO1 pathway, thereby reducing inflammation and apoptosis, processes that are critical for muscle regeneration. Additionally, treatment with PNU120596 or EA restores α7nAChR function and alleviates muscle atrophy. Our findings suggest that targeting α7nAChR offers a promising therapeutic approach for muscle wasting following denervation, with potential implications for clinical management and future intervention strategies.