Researchers have identified the genetic links between muscle atrophy and two types of myosin, paving the way for a new disease model for scientific research and potential new treatments.
The synergistic action of the muscle proteins myosin and actin enables skeletal muscle movements. The skeletal muscle myosin heavy chain or “MyHC” is a fundamental component of sarcomere – the basic contractile unit of muscle fibre.
Using a myosin double knockout mouse model, researchers from Japan recently discovered an association between skeletal muscle atrophy and the simultaneous absence of two types of MyHCs. Their findings could help clarify the molecular mechanisms underlying skeletal muscle wasting disorders.
Using mice that were simultaneously deficient for MyHC-IIx and MyHC-IIb, the research team, from the Division for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science at Fujita Health University, delineated the role of MyHC-IIx and MyHC-IIb in skeletal muscle atrophy.
“MyHC-IIx and MyHC-IIb are abundant in fast muscles and produce abundant instantaneous power. MyHC-IIb is barely detectable in human skeletal muscles. Mice deficient in these two types of MyHCs showed very severe muscle atrophy symptoms and died within the first four weeks of life,” said Dr Keisuke Hitachi of Fujita Health University, who planned the overall experimental design.
