骨格筋の負の調節因子への適応

骨格筋を減少させる調節因子に対する適応に関するサルコペニアと悪液質のレビュー論文を紹介します。

Kunihiro Sakuma and Akihiko Yamaguchi: Sarcopenia and cachexia: the adaptations of negative regulators of skeletal muscle mass. Journal of Cachexia, Sarcopenia and Muscle, DOI: 10.1007/s13539-011-0052-4

下記のHPで全文PDFで見れます。
http://www.springerlink.com/content/7k7234715q7k6766/fulltext.pdf

骨格筋の負の調節因子としてAtrogin-1、muscle ring finger-1、nuclear factor-kappaB (NF-κB)、myostatinなどが報告されていますが、どの調節因子が働いているかや調節因子に対する適応は、サルコペニアと悪液質では異なっています。この点に関して詳しくレビューしています。

特徴的なのがオートファジーに関する記載が少なからずあることです。サルコペニアと悪液質を語るには、オートファジーを知らなければいけない時代かもしれません。単にマイブームなだけかもしれませんが…。

Abstract
Recent advances in our understanding of the biology of muscle, and how anabolic and catabolic stimuli interact to control muscle mass and function, have led to new interest in the pharmacological treatment of muscle wasting. Loss of muscle occurs as a consequence of several chronic diseases (cachexia) as well as normal aging (sarcopenia). Although many negative regulators [Atrogin-1, muscle ring finger-1, nuclear factor-kappaB (NF-κB), myostatin, etc.] have been proposed to enhance protein degradation during both sarcopenia and cachexia, the adaptation of mediators markedly differs among these conditions. Sarcopenic and cachectic muscles have been demonstrated to be abundant in myostatin- and apoptosis-linked molecules. The ubiquitin–proteasome system (UPS) is activated during many different types of cachexia (cancer cachexia, cardiac heart failure, chronic obstructive pulmonary disease), but not many mediators of the UPS change during sarcopenia. NF-κB signaling is activated in cachectic, but not in sarcopenic, muscle. Some studies have indicated a change of autophagic signaling during both sarcopenia and cachexia, but the adaptation remains to be elucidated. This review provides an overview of the adaptive changes in negative regulators of muscle mass in both sarcopenia and cachexia.