Key result
mTORC1 inhibition in mice reveals its critical role regulating myofibril growth during mechanical overload.
Why the study?
Increased mechanical loading induces skeletal muscle growth and ultrastructural adaptations, but whether mTORC1 regulates myofibrillogenesis and the radial growth of myofibrils is unknown.
Does mTORC1 regulate myofibrillogenesis and radial growth of myofibrils in response to mechanical overload in mice?
Does mTORC1 regulate myofibrillogenesis and radial growth of myofibrils in response to mechanical overload in mice?
This preclinical study demonstrates that mTORC1 acts as a critical gatekeeper for ultrastructural adaptations, specifically myofibrillogenesis and radial growth, in skeletal muscle subjected to mechanical overload.
mTORC1 may regulate load-induced myofibrillogenesis; animal data leave open human relevance and therapeutic targeting.
Increased mechanical loading induces skeletal muscle growth and, at the ultrastructural level, promotes myofibrillogenesis and the radial growth of myofibrils. However, the mechanisms regulating these ultrastructural adaptations are not known. Here, we sought to determine whether the mechanistic target of rapamycin complex 1 (mTORC1) regulates these processes. To accomplish this, muscle-specific, tamoxifen-inducible raptor knockout (iRAmKO) mice were used to inhibit signaling through mTORC1, and growth was induced with a model of chronic mechanical overload (MOV). Using a next-generation fluorescence imaging pipeline for ultrastructural analyses, we found that mTORC1 is a critical regulator of the myofibrillogenesis and radial growth of myofibrils that occur in response to MOV. Together with other recent advances in the field, we propose a model in which mTORC1 acts as a gatekeeper that permits the retention, rather than the synthesis, of proteins that drive the ultrastructural adaptations.
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Flynn et al. (2026) studied Skeletal muscle growth. mTORC1 inhibition via raptor knockout was evaluated on Myofibrillogenesis and radial growth of myofibrils. Inhibition of mTORC1 signaling in mice demonstrated that mTORC1 is a critical regulator of myofibrillogenesis and radial growth of myofibrils in response to mechanical overload.
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