Abstract
Rho guanosine triphosphate hydrolases (GTPases) are molecular switches that cycle between an inactive guanosine diphosphate (GDP)-bound and an active guanosine triphosphate (GTP)-bound state during signal transduction. As such, they regulate a wide range of both cellular and physiological processes. In this review, we will summarize recent work on the role of Rho GTPase-regulated pathways in skeletal muscle development, regeneration, tissue mass homeostatic balance, and metabolism. In addition, we will present current evidence that links the dysregulation of these GTPases with diseases caused by skeletal muscle dysfunction. Overall, this information underscores the critical role of a number of members of the Rho GTPase subfamily in muscle development and the overall metabolic balance of mammalian species.
Highlights
Wellcome-MRC Institute of Metabolic Science and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge CB2 0QQ, UK
Previous studies have shown that Rho guanosine triphosphate hydrolases (GTPases) are relevant for both embryonic and adult myogenesis, periods in which they regulate processes linked to both cell fate specification and late skeletal myogenesis steps
Consistent with this role, a recent study has shown that the inactivation of the RhoA–ROCK axis caused by the depletion of the upstream exchange factor ArhGEF3 promotes injury-induced muscle regeneration by increasing autophagy in mice (Figure 4) [41]
Summary
Previous studies have shown that Rho GTPases are relevant for both embryonic and adult myogenesis, periods in which they regulate processes linked to both cell fate specification and late skeletal myogenesis steps. The activity of this GTPase must be shut down to prompt cell cycle withdrawal and the final myoblast fusion step [53,75,76,77] This latter step is mediated by the combined action of the Rho GAPs ArhGAP26 and.
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