骨骼肌消耗是严重烧伤高代谢的典型表现之一，严重影响患者的生存及预后。《Trends Endocrinol Metab》2013(12)文章等显示细胞自噬增强是骨骼肌消耗的重要因素之一， 而FoxO3是骨骼肌细胞中线粒体自噬的重要调控因子。但烧伤后FoxO3与线粒体自噬及骨骼肌消耗的相关性未见报道。《Burns》2013(6)文章及我们前期研究表明，烧伤可导致骨骼肌细胞线粒体结构功能紊乱、自噬增加以及FoxO3活性增高。因此， FoxO3可能通过调控线粒体自噬而影响烧伤后骨骼肌消耗。本课题拟：（1）探讨线粒体自噬与烧伤后骨骼肌消耗的关系；（2）明确烧伤后FoxO3对线粒体自噬的调控作用；（3）研究FoxO3是否通过FoxO3/Mul1/Mfn2、FoxO3/Bnip3等通路调控线粒体自噬进而影响严重烧伤后骨骼肌消耗。拟通过以上研究丰富严重烧伤后骨骼肌消耗发生的机制，为临床治疗提供理论依据。

Severe burns are typically followed by hypermetabolism that is characterized by significant muscle wasting, which causes considerable morbidity and mortality. Papers published in the Trends Endocrinol Metab 2013(12) and others indicate that enhancing autophagic activation is one of the important factors for skeletal muscle wasting, and FoxO3 plays a vital role in regulating mitophagy in skeletal muscle cell. However, the role of FoxO3a，mitophagy in severe burns-induced skeletal muscle wasting is still unknown. Paper published in Burns 2013(6) and our previous results demonstrate that severe burns could cause the damage of mitochondrial structure，mitochondrial dysfunction，mitophagy increases and FoxO3 higher expression in skeletal muscle. So, FoxO3 may have the role of regulation mitophagy, and then influence on skeletal muscle wasting post severe burns. The main research contents of this project include as follows: (1) to investigate the role of mitophagy in skeletal muscle wasting; (2) to evaluate the feasibility of FoxO3-mediated mitophagy in skeletal muscle post severe burns; (3) to reveal whether via FoxO3/Mul1/Mfn2, FoxO3/Bnip3 signaling pathway of mitophagy, FoxO3 has the role of regulating skeletal muscle wasting post severe burns. The results of this project may provide the theoretical foundation and potential target for clinical therapy of severe burns-induced skeletal muscle wasting.