脓毒症后获得性肌无力是临床难题，缺乏恰当模型深入研究。我们探索并改良模型发现21G穿刺针构建CLP后2周的小鼠可作为研究模型。结合体成分、称重及CSA发现股四头肌丢失最显著。转录组分析和验证提示肌肉再生受抑制，MYOD1显著下调；肌肉中FGF21特异性受体βKlotho上调。预测和验证后发现MYOD1转录因子STAT6上调。模型中米色脂肪增多，FGF21表达水平比其他组织高。细胞验证提示FGF21能够促进STAT6表达，抑制肌管形成。遂提出假说：米色脂肪通过FGF21/STAT6/MYOD1通路抑制肌肉再生诱发脓毒症后获得性肌无力。我们拟用腺相关病毒原位注射构建组织特异性过表达或敲减基因小鼠，从体内外探讨米色脂肪通过FGF21/STAT6/MYOD1抑制肌肉再生促进脓毒症后获得性肌无力。分析患者血清FGF21与股四头肌厚度、握力相关性，提供临床支撑。将为脓毒症后获得性肌无力防治提供新思路。

Acquired Muscle Weakness Post Sepsis is a difficult clinical problem which is lack of proper models for further study. We improved the model and found that mice with 2 weeks later after suffering CLP using 21G puncture needles could be used as research models. The most significant loss of quadriceps femoris was found in combination of body composition, weight and CSA. Transcriptome analysis and validation suggested that muscle regeneration was inhibited and MYOD1 was significantly downregulated. In the muscle, FGF21 specific receptor-βKlotho- is upregulated, and STAT6 was predicted as MYOD1 transcription factor by online software, which was upregulated in our research model.The beige adipose in the model was increased and the expression level of FGF21 was higher than other tissues. Cell research showed that FGF21 could promote STAT6 expression and inhibit the formation of muscle ducts. It was hypothesized that beige adipose inhibits muscle regeneration through the FGF21/STAT6/MYOD1 pathway in Acquire Muscle Weakness Post Sepsis. In this study, tissue-specific overexpression or knockdown gene in mice was constructed by in-situ injection of adeno-associated virus, and the mechanism of acquired muscle weakness after inhibition of muscle regeneration by beige adipose through FGF21/STAT6/MYOD1 was investigated in vivo and in vitro.The correlation between serum FGF21 and quadriceps thickness or grip strength was analyzed to provide clinical support.This will provide a new idea for the prevention and treatment of acquired muscle weakness post sepsis.