Bone and skeletal muscle: Key players in mechanotransduction and potential overlapping mechanisms

• We review the primary molecular mechanisms that have been implicated in skeletal muscle and bone mechanotransduction.
• mTORC1 signaling plays a fundamental role in the mechanical regulation of skeletal muscle mass and has several putative activators.
• GPCRs, ion channels, prostaglandins, IGF-1, Wnts and NO play roles in bone mechanostransduction.
• It remains to be determined whether mTORC1 signaling plays a role in the mechanical regulation of bone mass.
• It remains unknown whether prostaglandins and/or Wnts play a role in the mechanical activation of mTORC1 in skeletal muscle.

The development and maintenance of skeletal muscle and bone mass is critical for movement, health and issues associated with the quality of life. Skeletal muscle and bone mass are regulated by a variety of factors that include changes in mechanical loading. Moreover, bone mass is, in large part, regulated by muscle-derived mechanical forces and thus by changes in muscle mass/strength. A thorough understanding of the cellular mechanism(s) responsible for mechanotransduction in bone and skeletal muscle is essential for the development of effective exercise and pharmaceutical strategies aimed at increasing, and/or preventing the loss of, mass in these tissues. Thus, in this review we will attempt to summarize the current evidence for the major molecular mechanisms involved in mechanotransduction in skeletal muscle and bone. By examining the differences and similarities in mechanotransduction between these two tissues, it is hoped that this review will stimulate new insights and ideas for future research and promote collaboration between bone and muscle biologists.1