Talbert Erin E, Guttridge Denis C
Department of Molecular Virology, Immunology, and Medical Genetics, Human Cancer Genetics Program, and the Arthur G. James Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA.
Department of Molecular Virology, Immunology, and Medical Genetics, Human Cancer Genetics Program, and the Arthur G. James Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA.
Semin Cell Dev Biol. 2016 Jun;54:82-91. doi: 10.1016/j.semcdb.2015.09.009. Epub 2015 Sep 16.
While changes in muscle protein synthesis and degradation have long been known to contribute to muscle wasting, a body of literature has arisen which suggests that regulation of the satellite cell and its ensuing regenerative program are impaired in atrophied muscle. Lessons learned from cancer cachexia suggest that this regulation is simply not a consequence, but a contributing factor to the wasting process. In addition to satellite cells, evidence from mouse models of cancer cachexia also suggests that non-satellite progenitor cells from the muscle microenvironment are also involved. This chapter in the series reviews the evidence of dysfunctional muscle repair in multiple wasting conditions. Potential mechanisms for this dysfunctional regeneration are discussed, particularly in the context of cancer cachexia.
长期以来,人们已知肌肉蛋白质合成与降解的变化会导致肌肉萎缩,然而,有一批文献表明,萎缩肌肉中卫星细胞的调控及其后续的再生程序受到了损害。从癌症恶病质中吸取的教训表明,这种调控并非仅仅是一种结果,而是导致消瘦过程的一个促成因素。除了卫星细胞外,癌症恶病质小鼠模型的证据还表明,肌肉微环境中的非卫星祖细胞也参与其中。本系列的这一章回顾了多种消瘦病症中肌肉修复功能障碍的证据。讨论了这种功能失调再生的潜在机制,特别是在癌症恶病质的背景下。