Ogunbileje John O, Herndon David N, Murton Andrew J, Porter Craig
Department of Surgery, University of Texas Medical Branch, Galveston.
Mtabolism Unit, Shriners Hospitals for Children, Galveston, Texas.
J Burn Care Res. 2018 Jan 1;39(1):100-108. doi: 10.1097/BCR.0000000000000553.
Increased resting metabolic rate and skeletal muscle wasting are hallmarks of the pathophysiological stress response to severe burn trauma. However, whether these two responses occur independently in burn patients or are in fact related remains unclear. In light of recent evidence demonstrating that increased proteolysis in skeletal muscle of burned patients is accompanied by mitochondrial hypermetabolism, oxidative stress, and protein damage; in this article, we discuss the evidence for a role for the mitochondrion in skeletal muscle wasting following severe burn trauma. In particular, we focus on the role of mitochondrial superoxide production in oxidative stress and subsequent proteolysis, and discuss the role of the mitochondrion as a signaling organelle resulting in protein catabolism in other cellular compartments following severe burn trauma.
静息代谢率增加和骨骼肌消耗是严重烧伤创伤病理生理应激反应的标志。然而,这两种反应在烧伤患者中是独立发生还是实际上相互关联仍不清楚。鉴于最近有证据表明,烧伤患者骨骼肌中蛋白水解增加伴随着线粒体高代谢、氧化应激和蛋白质损伤;在本文中,我们讨论线粒体在严重烧伤创伤后骨骼肌消耗中作用的证据。特别是,我们关注线粒体超氧化物产生在氧化应激及随后蛋白水解中的作用,并讨论线粒体作为信号细胞器在严重烧伤创伤后导致其他细胞区室蛋白质分解代谢中的作用。