骨骼肌消耗是烧伤患者常见并发症之一，长期的骨骼肌消耗可增加患者感染几率、延迟创面愈合等，严重影响患者生活质量和预后。研究显示细胞自噬活性增强是诱发骨骼肌消耗的重要因素之一，而烧伤后心肌细胞、肝细胞和骨骼肌细胞等自噬水平明显升高。另外，研究还表明miRNA通过调控Akt/FoxO3a信号通路在肿瘤细胞、心肌细胞等的自噬过程中发挥重要作用。但miRNA在烧伤后骨骼肌细胞自噬及骨骼肌消耗中的作用还未见报道。课题组前期研究结果证实烧伤后大鼠骨骼肌中miR-190b低表达且细胞自噬明显增强，而Akt去磷酸化蛋白PHLPP1是miR-190b潜在作用靶点，且烧伤后PHLPP1表达明显升高。因此，miR-190b可能通过调控PHLPP1/Akt/FoxO3a通路而调控骨骼肌细胞自噬。本课题拟揭示miR-190b参与烧伤后骨骼肌细胞自噬及骨骼肌消耗的具体分子机制，为临床烧伤治疗提供理论依据及潜在作用靶点。

Skeletal muscle wasting is one of the common complications in burn patients. Long-term skeletal muscle wasting might increase the ratio of infection and delay wound healing, which seriously affected the qulity of life and prognosis. Reports indicate that enhancing autophagic activation is one of the important factors for skeletal muscle wasting. And autophagy of myocardial cell and skeletal muscle cell is elevated after burn injury. Furthermore, miRNA plays a pivotal role in autophagy of cancer cell and myocardial cell via regulating Akt/FoxO3a signal pathway. However, the role of miRNA in burn-induced cell autophagy and skeletal muscle wasting is still unknown. Our previous results demonstrate that miR-190b expression is suppressed and cell autophagy is increased in skeletal muscle after burn injury. PHLPP1, the potential target of miR-190b, is the phosphotase of Akt and overexpressed in skeletal muscle of burn rats. So miR-190b might mediate skeletal muscle cell autophagy through regulating PHLPP1/Akt/FoxO3a signal pathway. In this project, we want to reveal the mechanism of miR-190b involved in mediating skeletal muscle cell autophagy and skeletal muscle wasting, which might provide the theoritical foundation and potiential target for clinical therapy of burn-induced skeletal muscle wasting.