Zmynd17 controls muscle mitochondrial quality and whole-body metabolism

  • Ryo Fujita, Kiyoshi Yoshioka, Daiki Seko, Takashi Suematsu, Satomi Mitsuhashi, Nanami Senoo, Shinji Miura, Ichizo Nishino, Yusuke Ono
  • The FASEB Journal, September 2018, Federation of American Societies For Experimental Biology (FASEB)
  • DOI: 10.1096/fj.201701264r

What is it about?

Skeletal muscle is the largest tissue in the body, showing remarkable diversity and plasticity, and being responsible for locomotion as well as systemic energy storage and glucose metabolism. Approx¬imately 80% of postprandial blood glucose is cleared by skeletal muscle. Consequently, insulin-mediated muscle glucose uptake is central to maintaining systemic glucose homeostasis. Although recent evidence revealed that muscle mitochondria play a critical role in regulating systemic glucose homeostasis, it remains unclear how muscle mitochondria are maintained. Zmynd17 (also known as MSS51) was discovered in yeast and recently identified in mice and humans as a muscle-specific gene. However, the role of Zmynd17 is unknown. In this study, we demonstrate that Zmynd17 is a metabolic stress inducible regulator for systemic metabolism, which acts via mitochondrial quality control in muscle. This work provides new insights into the molecular basis of muscle mitochondrial homeostasis, and thus increasing Zmynd17 function may be a promising therapeutic approach for metabolic disorders such as insulin resistance and type 2 diabetes.

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The following have contributed to this page: Dr Yusuke Ono and Dr. Ryo Fujita